The DOI matches its Crossref record; 227 of the 230 references it cites were found in a registry or an index; 11 of the 197 sources its claims cite were checked for support.
Sleep and metabolic function
Open accessAbstract
Evidence for the role of sleep on metabolic and endocrine function has been reported more than four decades ago. In the past 30 years, the prevalence of obesity and diabetes has greatly increased in industrialized countries, and self-imposed sleep curtailment, now very common, is starting to be recognized as a contributing factor, alongside with increased caloric intake and decreased physical activity. Furthermore, obstructive sleep apnea, a chronic condition characterized by recurrent upper airway obstruction leading to intermittent hypoxemia and sleep fragmentation, has also become highly prevalent as a consequence of the epidemic of obesity and has been shown to contribute, in a vicious circle, to the metabolic disturbances observed in obese patients. In this article, we summarize the current data supporting the role of sleep in the regulation of glucose homeostasis and the hormones involved in the regulation of appetite. We also review the results of the epidemiologic and laboratory studies that investigated the impact of sleep duration and quality on the risk of developing diabetes and obesity, as well as the mechanisms underlying this increased risk. Finally, we discuss how obstructive sleep apnea affects glucose metabolism and the beneficial impact of its treatment, the continuous positive airway pressure. In conclusion, the data available in the literature highlight the importance of getting enough good sleep for metabolic health.
Overview
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TL;DR
This review summarizes evidence that sleep duration and quality modulate glucose homeostasis, appetite-regulating hormones, and risk of diabetes and obesity, with obstructive sleep apnea (OSA) as an additional metabolic risk. It concludes that sufficient good-quality sleep is important for metabolic health, while CPAP effects on glycemic control remain less clear-cut than for other cardiovascular risk factors.
Key findings
- Prospective epidemiologic studies indicate that short sleep (≤5–6 h/night), long sleep (>8–9 h/night), and sleep disturbances predict incident type 2 diabetes; pooled relative risks were 1.28 for short sleep, 1.48 for long sleep, 1.57 for difficulty initiating sleep, and 1.84 for difficulty maintaining sleep.
- Experimental partial sleep deprivation impaired insulin sensitivity in 7 of 11 studies and beta-cell dysfunction in 5 of 11; in one classic study, sleep debt decreased glucose tolerance by >40%, SI/AIRg/SG by ~25%, and disposition index by 50%.
- Sleep restriction altered appetite regulation: two nights of 4 h vs. 10 h in bed decreased leptin by 18%, increased ghrelin by 28%, increased the ghrelin/leptin ratio by >70%, and increased hunger by 23% and high-carbohydrate appetite by 33%.
- OSA is highly prevalent in type 2 diabetes (58–86% in polysomnography studies), and 17 of 35 studies reported improvement in at least one glucose-homeostasis parameter after CPAP, most consistently insulin sensitivity, though only five controlled studies existed and results were mixed.
Methods
- Narrative review of epidemiologic and experimental laboratory literature on sleep, glucose regulation, appetite hormones, obesity/diabetes risk, and OSA.
- Synthesizes cross-sectional, prospective, total sleep deprivation, partial sleep deprivation, sleep-fragmentation, and CPAP studies, with results presented in Tables 1–3 and figures.
- No primary data collection or formal systematic review methodology is described.
Limitations
- The paper states that future prospective epidemiologic studies need objective sleep measures, and that more controlled studies are necessary to evaluate CPAP effects on glucose homeostasis.
- The paper notes inconsistent leptin/ghrelin findings across studies and attributes these partly to differences in sample size, severity of sleep restriction, body composition, and OSA prevalence.
- Evident from the text: as a narrative review, it does not describe a systematic search strategy, inclusion criteria, or formal quality assessment of included studies.
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Claims the paper makes
104 Not checked yet · 18 Own interpretation · 7 No basis given · 4 Partly supported · 2 Supported · 1 Supported so far · 1 Own result · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Such phenomenon is observed for other weight promoting behaviors, notably physical inactivity and overeating, both of which are reinforced by weight gain [158].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Partly supportedcites [158] Sorensen TI (2009) Conference on “Multidisciplinary approaches to nutritional problems”. Symposium on “Diabetes and health”. Challenges in the study of causation of obesity. Proc Nutr Soc 68:43–54 sourceExperimental — accuracy not yet measured
The “Self-promoting weight gain” section reports that weight gain is associated with a subsequent decline in physical activity and increased food intake. But it describes continued self-promoting weight gain as a possible theoretical scenario, not an established vicious circle, and characterizes the increased intake as meeting higher energy needs rather than necessarily overeating. Page information is unavailable in our copy. (LLM, conf=0.86)
plainstates a cause- Asserted: passes — The authors put it forward as true.
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- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Of the 28 longitudinal studies that examined the impact of short sleep on obesity risk in children and adults, 22 reported that short sleep is associated with an increased risk of weight gain or development of obesity and/or increased fat mass a few years later”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Partly supportedcites [80] Knutson KL (2010) Sleep duration and cardiometabolic risk: a review of the epidemiologic evidence. Best Pract Res Clin Endocrinol Metab 24:731–743 sourceExperimental — accuracy not yet measured
The “Sleep and BMI, obesity and appetite regulation” section (page not provided) reports that many prospective studies in children and adults linked shorter sleep with later weight gain, obesity, or changes in body size. It does not report a tally of 28 longitudinal studies or say that 22 found an association; the follow-up periods it describes also vary, including a 16-year study. (LLM, conf=0.88)
- Partly supportedcites [8] Bo S et al (2011) Contributors to the obesity and hyperglycemia epidemics. A prospective study in a population-based cohort. Int J Obes. doi: 10.1038/ijo.2011.5 sourceExperimental — accuracy not yet measured
The Sleep restriction section (p. 11) reports that short sleep was associated with obesity at follow-up in this cohort and says other epidemiological studies have found an association. It does not report a review of 28 longitudinal studies, the 22-study count, or findings spanning children and adults, weight gain, and fat mass. (LLM, conf=0.86)
- Partly supportedcites [21] Carter PJ, Taylor BJ, Williams SM, Taylor RW (2011) Longitudinal analysis of sleep in relation to BMI and body fat in children: the FLAME study. BMJ 342:d2712 sourceExperimental — accuracy not yet measured
The Introduction (page not supplied) reports a relatively consistent link between shorter sleep and childhood overweight, and the Discussion (page not supplied) reports greater fat-mass gain among children who slept less. The paper does not report that 22 of 28 longitudinal studies found this association across children and adults; its Introduction instead mentions eight recent prospective studies in the childhood literature. (LLM, conf=0.88)
- Not checked yetcites [38] Diethelm K, Bolzenius K, Cheng G, Remer T, Buyken AE (2011) Longitudinal associations between reported sleep duration in early childhood and the development of body mass index, fat mass index and fat free mass index until age 7. Int J Pediatr Obes 6:e114–e123 source
- Not checked yetcites [89] Landhuis CE, Poulton R, Welch D, Hancox RJ (2008) Childhood sleep time and long-term risk for obesity: a 32-year prospective birth cohort study. Pediatrics 122:955–960 source
- Not checked yetcites [94] Littman AJ et al (2007) Sleep, ghrelin, leptin and changes in body weight during a 1-year moderate-intensity physical activity intervention. Int J Obes 31:466–475 source
- Not checked yetcites [97] Lyytikainen P, Rahkonen O, Lahelma E, Lallukka T (2011) Association of sleep duration with weight and weight gain: a prospective follow-up study. J Sleep Res 20:298–302 source
- Not checked yetcites [101] Marshall NS et al (2010) Changes in sleep duration and changes in weight in obese patients: the Swedish obese subjects study. Sleep Biol Rhythms 8:63–71 source
- Partly supportedcites [105] Mozaffarian D, Hao T, Rimm EB, Willett WC, Hu FB (2011) Changes in diet and lifestyle and long-term weight gain in women and men. N Engl J Med 364:2392–2404 sourceExperimental — accuracy not yet measured
The Results and Discussion report an association between shorter sleep and greater weight gain, and the Discussion notes that some prospective studies support a link with obesity. Neither section reports a review of 28 longitudinal studies, a finding in 22 of them, or the claimed combined findings for children and adults. Page numbers are unavailable in our copy. (LLM, conf=0.88)
- Partly supportedcites [120] Nishiura C, Hashimoto H (2010) A 4-year study of the association between short sleep duration and change in body mass index in Japanese male workers. J Epidemiol 20:385–390 sourceExperimental — accuracy not yet measured
The Results and Discussion report an association between short sleep and relative BMI increase over four years in Japanese male workers. The paper does not report a tally of 28 longitudinal studies or say that 22 found increased weight gain, obesity, or fat mass in children and adults. (LLM, conf=0.84)
plainstates an association- Asserted: passes — The authors put it forward as true.
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- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Two studies have demonstrated that poor sleep quality, independently of sleep duration, impairs glucose regulation in healthy young adults [167, 176].”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Supportedcites [167] Stamatakis KA, Punjabi NM (2010) Effects of sleep fragmentation on glucose metabolism in normal subjects. Chest 137:95–101 source
The Discussion reports that two nights of fragmented sleep reduced measures of glucose regulation by 20%–25% while sleep duration was preserved. The study used healthy, younger volunteers (Discussion), and the paper also describes a second study reporting worsened insulin resistance after selective suppression of slow-wave sleep (Heart Rate Variability Analysis). (LLM, conf=0.91)
- Not checked yetcites [176] Tasali E, Leproult R, Ehrmann DA, Van Cauter E (2008) Slow-wave sleep and the risk of type 2 diabetes in humans. Proc Natl Acad Sci USA 105:1044–1049 source
boostedstates a cause- Asserted: passes — The authors put it forward as true.
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“and 1.55 (95% CI, 1.43–1.68; p<0.0001) in adults [18].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Supportedcites [18] Cappuccio FP et al (2008) Meta-analysis of short sleep duration and obesity in children and adults. Sleep 31:619–626 source
The adults section reports a pooled odds ratio of 1.55 (95% CI, 1.43–1.68) for short sleep duration and obesity. The Abstract also gives P < 0.0001 for the adult estimate, matching the citing sentence. (LLM, conf=0.95)
plainstates an association- Asserted: passes — The authors put it forward as true.
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- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In a study that assessed the 24-h leptin profiles after 6 days of 4-, 8-, and 12-h bedtimes in healthy lean young men under conditions of stable caloric intake and activity levels, all characteristics of the 24-h leptin profile (overall mean, nocturnal maximum, and amplitude) gradually increased from the 4- to the 12-h bedtime condition [161].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Partly supportedcites [161] Spiegel K et al (2004) Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. J Clin Endocrinol Metabol 89:5762–5771 sourceExperimental — accuracy not yet measured
The Leptin results report higher 24-hour mean, nocturnal peak, and amplitude with 12-h than with 4-h bedtimes despite similar caloric intake and activity. The Correlations section says the 8-h leptin data were intermediate, supporting the overall trend. However, the Experimental protocol says the 8-h profiles came from a separate study of nine subjects one year later, not from six days in an 8-h condition alongside the 4-h and 12-h conditions. (LLM, conf=0.86)
plainstates a cause- Asserted: passes — The authors put it forward as true.
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- Partly supported
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“a dose–response relationship between slow wave activity (SWA) and the amount of GH secreted has been evidenced in young and older men.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
boostedstates an association- Asserted: passes — The authors put it forward as true.
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In the paper
“conversely, total sleep deprivation leads to marked hyperphagia [133].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Appetite regulation and sleep
What the sources say
- Not checked yetcites [133] Rechtschaffen A, Bergmann BM (1995) Sleep deprivation in the rat by the disk-over-water method. Behav Brain Res 69:55–63 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“SWS, which is particularly abundant at the beginning of the sleep period, has been shown to result in a 30–40% decrease in cerebral glucose metabolism relative to waking or rapid eye movement (REM) sleep [12].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [12] Boyle PJ et al (1994) Diminished brain glucose metabolism is a significant determinant for falling rates of systemic glucose utilization during sleep in normal humans. J Clin Invest 93:529–535 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“Both nocturnal and daytime sleeps were associated with a marked decrease in glucose tolerance, reflected by increased glucose levels.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [187] Van Cauter E et al (1991) Modulation of glucose regulation and insulin secretion by circadian rhythmicity and sleep. J Clin Invest 88:934–942 source
plainstates an association- Asserted: passes — The authors put it forward as true.
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In the paper
“In rodents, food shortage or starvation results in decreased sleep [35]”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Appetite regulation and sleep
What the sources say
- Not checked yetcites [35] Danguir J, Nicolaidis S (1979) Dependence of sleep on nutrients’ availability. Physiol Behav 22:735–740 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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- It may state two separate claims as one. 44
- Probably not a substantial claim. 5
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Thus, of the three studies that assessed SI after a glucose load, two found reduced SI after sleep loss [5, 195] and one found reduced SI after recovery sleep [204].”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [5] Benedict C et al (2011) Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr 93:1229–1236 source
- Not checked yetcites [195] VanHelder T, Symons JD, Radomski MW (1993) Effects of sleep deprivation and exercise on glucose tolerance. Aviat Space Environ Med 64:487–492
- Partly supportedcites [204] Wehrens SM, Hampton SM, Finn RE, Skene DJ (2010) Effect of total sleep deprivation on postprandial metabolic and insulin responses in shift workers and non-shift workers. J Endocrinol 206:205–215 sourceExperimental — accuracy not yet measured
The Discussion reports a larger postprandial insulin response after recovery sleep despite similar glucose levels, which the authors interpret as insulin insensitivity. However, they tested responses to a standard breakfast, not a glucose load, and inferred insulin sensitivity from those responses rather than directly measuring it. The other two studies in the citing sentence are attached to different citations. (LLM, conf=0.85)
plainstates a cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“In this latter study, however, the DI was not affected by the sleep fragmentation since an increase in insulin release was able to compensate the decrease in SI.”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Supportedcites [167] Stamatakis KA, Punjabi NM (2010) Effects of sleep fragmentation on glucose metabolism in normal subjects. Chest 137:95–101 source
The IVGTT results passage (indexed under Heart Rate Variability Analysis; page unavailable) reports that insulin sensitivity decreased and the acute insulin response increased after sleep fragmentation. It explicitly links those changes to a disposition index that was numerically lower but not statistically different from baseline (P = .37), supporting the claim in the statistical sense. (LLM, conf=0.88)
plainstates a cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Supported
In the paper
“in healthy young men, a major GH pulse that accounts for roughly 70% of the daily production occurs shortly after sleep onset [188], in association with the first phase of slow wave sleep (SWS).”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [188] Van Cauter E et al (1992) A quantitative estimation of growth hormone secretion in normal man: reproducibility and relation to sleep and time of day. J Clin Endocrinol Metabol 74:1441–1450 source
plainstates an association- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“wake–sleep and sleep–wake transitions are associated with inhibition and stimulation of cortisol levels, respectively [59, 168, 186].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [59] Gronfier C, Brandenberger G (1998) Ultradian rhythms in pituitary and adrenal hormones: their relations to sleep. Sleep Med Rev 2:17–29 source
- Not checked yetcites [168] Steiger A (2003) Sleep and endocrinology. J Intern Med 254:13–22 source
- Not checked yetcites [186] Van Cauter E (2005) Endocrine physiology. In: Kryger M, Roth T, Dement WC (eds) Principles and practice of sleep medicine, 4th edn. Elsevier-Saunders, Philadelphia
plainstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“A glucose and insulin elevation of roughly half the amplitude of the one observed during nocturnal sleep was apparent during the night of sleep deprivation, indicating that circadian-dependent processes also modulate glucose regulation.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [187] Van Cauter E et al (1991) Modulation of glucose regulation and insulin secretion by circadian rhythmicity and sleep. J Clin Invest 88:934–942 source
hedgedstates an association- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“GH levels are increased during sleep, irrespective of the time at which sleep occurs, and they are markedly diminished during sleep deprivation.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [151] Simon C, Brandenberger G, Follenius M (1987) Ultradian oscillations of plasma glucose, insulin, and C-peptide in man during continuous enteral nutrition. J Clin Endocrinol Metabol 64:669–674 source
- Not checked yetcites [152] Simon C, Brandenberger G, Saini J, Ehrhart J, Follenius M (1994) Slow oscillations of plasma glucose and insulin secretion rate are amplified during sleep in humans under continuous enteral nutrition. Sleep 17:333–338 source
- Not checked yetcites [187] Van Cauter E et al (1991) Modulation of glucose regulation and insulin secretion by circadian rhythmicity and sleep. J Clin Invest 88:934–942 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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In the paper
“In the study by Benedict et al. [5], the decreased glucose tolerance in a state of sleep debt was the consequence of reduced SI combined to beta-cell dysfunction since insulin levels were not affected by the presence or absence of sleep.”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [5] Benedict C et al (2011) Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr 93:1229–1236 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Glucose tolerance during this ivGTT was decreased by more than 40% when the subjects were in a state of sleep debt and reached values typical for older adults with impaired glucose tolerance [54].”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [54] Garcia G et al (1997) Glucose metabolism in older adults: a study including subjects more than 80 years of age. J Am Geriatr Soc 45:813–817 source
plainstates a causen = 11- Asserted: passes — The authors put it forward as true.
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In the paper
“Short sleep duration (mostly ≤5and/or ≤6h) was found to predict a higher incidence of diabetes in seven of the nines studies, while poor sleep quality was associated with an increased risk of diabetes in five of the six studies [80].”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Epidemiologic evidence
What the sources say
- Not checked yetcites [80] Knutson KL (2010) Sleep duration and cardiometabolic risk: a review of the epidemiologic evidence. Best Pract Res Clin Endocrinol Metab 24:731–743 source
plainstates an association- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Glucose tolerance was found to be altered in two studies, i.e., after 72–126 h of TSD [86] and after 24 h of TSD [5].”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [86] Kuhn E, Brodan V, Brodanova M, Rysanek K (1969) Metabolic reflection of sleep deprivation. Act Nerv Super (Praha) 11:165–174
- Not checked yetcites [5] Benedict C et al (2011) Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr 93:1229–1236 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Increased fasting glucose was reported after 120 h of TSD [200] but not after 72–126 h [86] or one single night of TSD [5, 143, 195, 204]”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [200] Vondra K et al (1981) Effects of sleep deprivation on the activity of selected metabolic enzymes in skeletal muscle. Eur J Appl Physiol Occup Physiol 47:41–46 source
- Not checked yetcites [86] Kuhn E, Brodan V, Brodanova M, Rysanek K (1969) Metabolic reflection of sleep deprivation. Act Nerv Super (Praha) 11:165–174
- Not checked yetcites [5] Benedict C et al (2011) Acute sleep deprivation reduces energy expenditure in healthy men. Am J Clin Nutr 93:1229–1236 source
- Not checked yetcites [143] Schmid SM et al (2007) Sleep loss alters basal metabolic hormone secretion and modulates the dynamic counterregulatory response to hypoglycemia. J Clin Endocrinol Metabol 92:3044–3051 source
- Not checked yetcites [195] VanHelder T, Symons JD, Radomski MW (1993) Effects of sleep deprivation and exercise on glucose tolerance. Aviat Space Environ Med 64:487–492
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“All [95, 166] but one [3] of the studies that have attempted to characterize the overnight profiles of acylated ghrelin in relation to unacylated ghrelin confirmed the increased nocturnal elevation in total ghrelin and demonstrated a concomitant increase in acylated ghrelin.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Appetite regulation and sleep
What the sources say
- Not checked yetcites [95] Liu J et al (2008) Novel ghrelin assays provide evidence for independent regulation of ghrelin acylation and secretion in healthy young men. J Clin Endocrinol Metabol 93:1980–1987 source
- Not checked yetcites [166] Spiegel K, Tasali E, Leproult R, Scherberg N, Van Cauter E (2011) Twenty-four-hour profiles of acylated and total ghrelin: relationship with glucose levels and impact of time of day and sleep. J Clin Endocrinol Metabol 96:486–493 source
- Not checked yetcites [3] Avram AM, Jaffe CA, Symons KV, Barkan AL (2005) Endogenous circulating ghrelin does not mediate growth hormone rhythmicity or response to fasting. J Clin Endocrinol Metabol 90:2982–2987 source
boostedstates an association- Asserted: passes — The authors put it forward as true.
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In the paper
“and an OR of 1.92 (95% CI, 1.15–3.2) in children with the shortest sleep duration, suggesting a dose–response relationship between sleep duration increased risk of obesity [23].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Not checked yetcites [23] Chen X, Beydoun MA, Wang Y (2008) Is sleep duration associated with childhood obesity? A systematic review and meta-analysis. Obesity (Silver Spring, Md) 16:265–274 source
hedgedstates an association- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Studies in adults are less consistent and often show a U-shaped relationship between sleep duration and BMI.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
plainstates an association- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“However, there were only five controlled studies among those published in literature, of which three yielded positive results, while the other two were unable to demonstrate a beneficial impact of CPAP on glucose homeostasis.”
§ Sleep and metabolic function > Obstructive sleep apnea and type 2 diabetes
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“The number of adults aged 25 years or older with diabetes has more than doubled over nearly three decades and is currently approaching 350 million [34].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [34] Danaei G et al (2011) National, regional, and global trends in fasting plasma glucose and diabetes prevalence since 1980: systematic analysis of health examination surveys and epidemiological studies with 370 country-years and 2.7 million participants. Lancet 378:31–40 source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“glucose tolerance, the 24-h pattern of release of insulin, and the counterregulatory hormones growth hormone (GH) and cortisol, as well as of hormones involved in the regulation of appetite, such as leptin and ghrelin, are partly dependent on sleep timing, duration, and quality [59, 168, 186].”
§ Sleep and metabolic function > Introduction
What the sources say
- Not checked yetcites [59] Gronfier C, Brandenberger G (1998) Ultradian rhythms in pituitary and adrenal hormones: their relations to sleep. Sleep Med Rev 2:17–29 source
- Not checked yetcites [168] Steiger A (2003) Sleep and endocrinology. J Intern Med 254:13–22 source
- Not checked yetcites [186] Van Cauter E (2005) Endocrine physiology. In: Kryger M, Roth T, Dement WC (eds) Principles and practice of sleep medicine, 4th edn. Elsevier-Saunders, Philadelphia
plainstates a possible cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Type 2 diabetes is a complex metabolic disorder that involves insulin resistance, impaired insulin secretion, and increased glucose production [37, 79].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [37] DeFronzo RA (2004) Pathogenesis of type 2 diabetes mellitus. Med Clin North Am 88:787–835, ix source
- Not checked yetcites [79] Kahn SE (2003) The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of type 2 diabetes. Diabetologia 46:3–19 source
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Voluntary sleep curtailment has, indeed, become an increasingly common behavior in all age groups over the past several decades, most likely reflecting the demands and opportunities of modern society [75, 114].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
What the sources say
- Not checked yetcites [75] Institut National de Prévention et d’Education pour la Santé. Les français et leur sommeil. http://www.inpes.sante.fr/70000/dp/08/dp080310.pdf . 1–45.
- Not checked yetcites [114] National Sleep Foundation (2008) “Sleep in America” Poll. http://www.sleepfoundation.org./sites/default/files/2008%20POLL%20SOF.PDF . 1–45
plainstates an association- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, glucose regulation is markedly influenced by circadian rhythmicity and sleep, and these effects could be partially mediated by cortisol and GH.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Glucose regulation and sleep
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In contrast to leptin, ghrelin stimulates hunger and food intake, reduces EE, and promotes the retention of fat [56, 58, 92, 191].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Appetite regulation and sleep
What the sources say
- Not checked yetcites [56] Gasco V et al (2010) Endocrine and metabolic actions of ghrelin. Endocr Dev 17:86–95 source
- Not checked yetcites [58] Granata R, Baragli A, Settanni F, Scarlatti F, Ghigo E (2010) Unraveling the role of the ghrelin gene peptides in the endocrine pancreas. J Mol Endocrinol 45:107–118 source
- Not checked yetcites [92] Lim CT, Kola B, Korbonits M, Grossman AB (2010) Ghrelin’s role as a major regulator of appetite and its other functions in neuroendocrinology. Prog Brain Res 182:189–205 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“These findings support an inhibitory effect of sleep on ghrelin, consistent with the association between sleeping and fasting and, conversely, between feeding and arousal.”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Appetite regulation and sleep
What the sources say
- Not checked yetcites [166] Spiegel K, Tasali E, Leproult R, Scherberg N, Van Cauter E (2011) Twenty-four-hour profiles of acylated and total ghrelin: relationship with glucose levels and impact of time of day and sleep. J Clin Endocrinol Metabol 96:486–493 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
- Rests on an assumption: Feeding and sleeping are mutually exclusive.
None of the sources cited for this claim have been checked yet.
In the paper
“Leptin inhibits hunger and food intake, increases EE, and promotes fat utilization [1, 193].”
§ Sleep and metabolic function > Sleep modulates glucose regulation and hormones involved in appetite regulation > Appetite regulation and sleep
What the sources say
- Not checked yetcites [1] Ahima RS, Saper CB, Flier JS, Elmquist JK (2000) Leptin regulation of neuroendocrine systems. Front Neuroendocrinol 21:263–307 source
- Not checked yetcites [193] van Dijk G (2001) The role of leptin in the regulation of energy balance and adiposity. J Neuroendocrinol 13:913–921 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“To note, one prospective study in adults reported a bidirectional relationship between short sleep and obesity; not only did short sleep predict weight gain a few years later [67], but body weight or obesity also predicted short sleep duration on a later occasion.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Not checked yetcites [67] Hasler G et al (2004) The association between short sleep duration and obesity in young adults: a 13-year prospective study. Sleep 27:661–666 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Taken together, these results suggest the existence of a “vicious circle” where short sleep may initially promote weight gain, and the resulting excess adiposity would then induce sleep disturbances, with a further decrease in total sleep time.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
hedgedstates a cause- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, overall, the impact of reduced sleep duration on obesity risk is particularly clear in pediatric populations, probably because physiological and behavioral mechanisms responsible for this association are stronger in younger ages.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
hedgedstates an association- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The physiological and behavioral mechanisms linking short sleep to obesity are stronger at younger ages.
None of the sources cited for this claim have been checked yet.
In the paper
“However, even modest increases in weight have been shown to have significant implications for long-term adiposity-related metabolic dysfunction, diabetes, cardiovascular disease, and cancer [28, 46, 135, 208].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Not checked yetcites [28] Colditz GA, Willett WC, Rotnitzky A, Manson JE (1995) Weight gain as a risk factor for clinical diabetes mellitus in women. Ann Intern Med 122:481–486 source
- Not checked yetcites [46] Eliassen AH, Colditz GA, Rosner B, Willett WC, Hankinson SE (2006) Adult weight change and risk of postmenopausal breast cancer. JAMA 296:193–201 source
- Not checked yetcites [135] Rexrode KM et al (1997) A prospective study of body mass index, weight change, and risk of stroke in women. JAMA 277:1539–1545 source
- Not checked yetcites [208] Willett WC et al (1995) Weight, weight change, and coronary heart disease in women. Risk within the ‘normal’ weight range. JAMA 273:461–465 source
boostedstates an association- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“U- or L-shaped associations were reported in some adult prospective studies (reviewed in [80]; additional studies: [97, 202]); hence, the relationship between longer sleep and BMI is conflicting in adults and inexistent in children.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Not checked yetcites [80] Knutson KL (2010) Sleep duration and cardiometabolic risk: a review of the epidemiologic evidence. Best Pract Res Clin Endocrinol Metab 24:731–743 source
- Not checked yetcites [97] Lyytikainen P, Rahkonen O, Lahelma E, Lallukka T (2011) Association of sleep duration with weight and weight gain: a prospective follow-up study. J Sleep Res 20:298–302 source
- Not checked yetcites [202] Watanabe M, Kikuchi H, Tanaka K, Takahashi M (2010) Association of short sleep duration with weight gain and obesity at 1-year follow-up: a large-scale prospective study. Sleep 33:161–167 source
plainstates an association- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“It is possible that weight is not gained linearly over the course of the short sleeping period. As a consequence, “in order for short sleep to predict any physiological or behavioral change, the longitudinal time frame examined would need to start prior to or at the beginning of the short sleep transition for each participant” [98], which is less likely to be the case with older ages.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Epidemiologic evidence
What the sources say
- Not checked yetcites [98] Magee L, Hale L (2011) Longitudinal associations between sleep duration and subsequent weight gain: a systematic review. Sleep Med Rev. doi: 10.1016/j.smrv.2011.05.005 source
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- The authors state this as an assumption: Weight is not gained linearly over the course of a short sleeping period.
In the paper
“In the general population, the prevalence of OSA is around 17% [215].”
§ Sleep and metabolic function > Obstructive sleep apnea and type 2 diabetes
What the sources say
- Not checked yetcites [215] Young T, Peppard PE, Taheri S (2005) Excess weight and sleep-disordered breathing. J Appl Physiol 99:1592–1599 source
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“At the end of the 2 weeks of sleep curtailment, the proportion of weight lost as fat was decreased by 55%, and the loss of fat-free body mass was increased by 60%.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [117] Nedeltcheva AV, Kilkus JM, Imperial J, Schoeller DA, Penev PD (2010) Insufficient sleep undermines dietary efforts to reduce adiposity. Ann Intern Med 153:435–441 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Conversely, no impact of TSD was evidenced in another recent study that also reported reduced amplitude of the 24-h leptin diurnal variation due to increased daytime leptin levels [126].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [126] Pejovic S et al (2010) Leptin and hunger levels in young healthy adults after one night of sleep loss. J Sleep Res 19:552–558 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Of note, the study of St-Onge et al. reported an increase of ~300 kcal/day after 5 days of 4 h bedtimes, although there was no clear effect of sleep duration on subjective feelings of hunger and appetite on the previous day [11, 170], suggesting that subjective assessments are unreliable.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [11] Bosy-Westphal A et al (2008) Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women. Obes Facts 1:266–273 source
- Not checked yetcites [170] St-Onge MP et al (2011) Short sleep duration increases energy intakes but does not change energy expenditure in normal-weight individuals. Am J Clin Nutr 94:410–416 source
hedgedstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“As leptin levels are enhanced by food intake and correlate with the degree of obesity [25], these latter results may be the expected consequence of the positive energy balance achieved by increased food intake [11, 116, 146] and weight gain [11, 116].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [25] Chin-Chance C, Polonsky KS, Schoeller DA (2000) Twenty-four-hour leptin levels respond to cumulative short-term energy imbalance and predict subsequent intake. J Clin Endocrinol Metabol 85:2685–2691 source
- Not checked yetcites [11] Bosy-Westphal A et al (2008) Influence of partial sleep deprivation on energy balance and insulin sensitivity in healthy women. Obes Facts 1:266–273 source
- Not checked yetcites [116] Nedeltcheva AV et al (2009) Sleep curtailment is accompanied by increased intake of calories from snacks. Am J Clin Nutr 89:126–133 source
- Not checked yetcites [146] Schmid SM et al (2009) Short-term sleep loss decreases physical activity under free-living conditions but does not increase food intake under time-deprived laboratory conditions in healthy men. Am J Clin Nutr 90:1476–1482 source
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Again, this unlimited availability of palatable food resulted in overeating (+60% regardless of the bedtime condition) and may have masked the impact of sleep loss on food consumption [146].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [146] Schmid SM et al (2009) Short-term sleep loss decreases physical activity under free-living conditions but does not increase food intake under time-deprived laboratory conditions in healthy men. Am J Clin Nutr 90:1476–1482 source
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“One pathway that may link short sleep to excess weight is increased caloric intake in short sleepers.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
In the paper
“For example, in the study that submitted the subjects to caloric restriction, leptin levels declined in parallel with the loss of weight and adiposity without a significant independent effect of sleep loss: The negative energy balance most likely overrode the impact of sleep duration [117].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [117] Nedeltcheva AV, Kilkus JM, Imperial J, Schoeller DA, Penev PD (2010) Insufficient sleep undermines dietary efforts to reduce adiposity. Ann Intern Med 153:435–441 source
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“By contrast, Nedeltcheva et al. observed similar weight at the end of each 14-day period of sleep extension or sleep restriction in overweight men and women exposed to unlimited palatable food in a laboratory setting. Consistent with the fact that overeating usually occurs when unlimited palatable food is available [132], the subjects overate and gained ~2 kg in each sleep condition [116].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [116] Nedeltcheva AV et al (2009) Sleep curtailment is accompanied by increased intake of calories from snacks. Am J Clin Nutr 89:126–133 source
- Not checked yetcites [132] Raynor HA, Wing RR (2007) Package unit size and amount of food: do both influence intake? Obesity (Silver Spring Md) 15:2311–2319 source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Leptin decreased by 18%, while ghrelin increased by 28%, and the ghrelin/leptin ratio increased by more than 70% when sleep was restricted (Fig. 3).”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [162] Spiegel K, Tasali E, Penev P, Van Cauter E (2004) Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med 141:846–850 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Accordingly, in the study by Benedict et al., ghrelin was higher in the second half of the night compared to a night of normal sleep, whereas nighttime leptin levels were unchanged.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Importantly, in the latter two studies, EE measured with the gold standard doubly labeled water method did not differ between study conditions, therefore suggesting that the increase in food consumption most often associated with sleep loss is not related to a comparable rise in energy needs and would eventually result in a positive energy balance.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
hedgedstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In overweight middle-aged adults, increased consumption of calories from snacks with higher carbohydrate content was observed after 2 weeks of sleep restriction (−1.5 h/night) in comparison to after 2 weeks of sleep extension (+1.5 h/night), while energy intake from meal and total energy intake were unaffected by bedtime condition [116].”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [116] Nedeltcheva AV et al (2009) Sleep curtailment is accompanied by increased intake of calories from snacks. Am J Clin Nutr 89:126–133 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, increased ghrelin levels and elevated hunger scores were observed in the sleep restriction condition, suggesting that, in contrast to what was observed with leptin, sleep loss was able to exacerbate the upregulation of ghrelin and hunger triggered by a negative energy balance.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
hedgedstates a possible cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The state of sleep loss also resulted in a 23% increase in hunger and in a 33% increase in appetite for nutrients with high carbohydrate content.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [162] Spiegel K, Tasali E, Penev P, Van Cauter E (2004) Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med 141:846–850 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“By comparison, 3 days of underfeeding by approximately 900 cal/day in healthy lean volunteers resulted in a 22% decrease of leptin levels [25]; these results highlight the functional significance of the decrease in leptin observed with sleep loss.”
§ Sleep and metabolic function > Short sleep as risk factor of obesity > Evidence from experimental laboratory studies
What the sources say
- Not checked yetcites [25] Chin-Chance C, Polonsky KS, Schoeller DA (2000) Twenty-four-hour leptin levels respond to cumulative short-term energy imbalance and predict subsequent intake. J Clin Endocrinol Metabol 85:2685–2691 source
plainstates a cause- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Methodological differences may also account for the variability of results obtained: four positive studies relied on the hyperinsulinemic–euglycemic clamp technique to assess SI [15, 65, 66, 142], which is considered the gold standard to evaluate SI; another two used continuous glucose monitoring (CGMS) [4, 205], which provides 288 readings of interstitial glucose levels per 24 h (every 5 min) and”
§ Sleep and metabolic function > Obstructive sleep apnea and type 2 diabetes
What the sources say
- Not checked yetcites [15] Brooks B et al (1994) Obstructive sleep apnea in obese noninsulin-dependent diabetic patients: effects of continuous positive airway pressure treatment on insulin responsiveness. J Clin Endocrinol Metabol 79:1681–1685 source
- Not checked yetcites [65] Harsch IA et al (2004) Continuous positive airway pressure treatment rapidly improves insulin sensitivity in patients with obstructive sleep apnea syndrome. Am J Respir Crit Care Med 169:156–162 source
- Not checked yetcites [66] Harsch IA et al (2004) The effect of continuous positive airway pressure treatment on insulin sensitivity in patients with obstructive sleep apnoea syndrome and type 2 diabetes. Respiration 71:252–259 source
- Not checked yetcites [142] Schahin SP et al (2008) Long-term improvement of insulin sensitivity during CPAP therapy in the obstructive sleep apnoea syndrome. Med Sci Mon 14:CR117–CR121
- Not checked yetcites [4] Babu AR, Herdegen J, Fogelfeld L, Shott S, Mazzone T (2005) Type 2 diabetes, glycemic control, and continuous positive airway pressure in obstructive sleep apnea. Arch Intern Med 165:447–452 source
- Not checked yetcites [205] Wei CY et al (2009) Effects of continuous positive airway pressure upon 24 h changes of blood glucose level in patients with obstructive sleep apnea hypopnea syndrome and type 2 diabetes. Zonghua Yi Xue Yi Chuan Xue Za Zi 89:2686–2689
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“HOMA-IR has been found to correlate reasonably well with the glucose clamp and minimal model estimates of insulin sensitivity/resistance in several studies of distinct populations. However, it is a measure of basal insulin sensitivity/resistance and does not provide information about dynamic conditions [201].”
§ Sleep and metabolic function > Obstructive sleep apnea and type 2 diabetes
What the sources say
- Not checked yetcites [201] Wallace TM, Levy JC, Matthews DR (2004) Use and abuse of HOMA modeling. Diabetes Care 27:1487 source
plainstates an association- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: HOMA-IR correlates reasonably well with the glucose clamp and minimal model estimates of insulin sensitivity/resistance.
The paper relies on this without support.
Feeding and sleeping are mutually exclusive.
“Feeding and sleeping are mutually exclusive: They are both time-consuming and occur in cyclic patterns.”
The paper relies on this without support.
In healthy subjects, insulin resistance is accompanied by compensatory hyperinsulinemia that maintains a constant disposition index.
“In healthy subjects, insulin resistance is accompanied by compensatory hyperinsulinemia, which in turn maintains a constant DI.”
The paper relies on this without support.
Sympathetic activation inhibits insulin release and parasympathetic activation stimulates it.
“Sympathetic activation inhibits and para-sympathetic activation stimulates insulin release”
The paper relies on this without support.
Aging and obstructive sleep apnea are recognized risk factors for decreased glucose tolerance and increased diabetes risk.
“Both aging and OSA are recognized risk factors for decreased glucose tolerance and increased diabetes risk.”
The paper relies on this without support.
PYY inhibits appetite.
“In contrast to ghrelin, PYY inhibits appetite.”
The paper relies on this without support.
Modern lifestyle of physical inactivity and increased food intake contributes to the growing prevalence of type 2 diabetes worldwide.
“If it is obvious that our modern lifestyle of physical inactivity and increased food intake is involved in the growing prevalence of type 2 diabetes worldwide”
The paper relies on this without support.
The prevalence of sleep disorders, particularly obstructive sleep apnea, has greatly increased, although they often remain undiagnosed.
“In addition, the prevalence of sleep disorders, particularly obstructive sleep apnea (OSA), has greatly increased, although they often remain undiagnosed.”
The paper relies on this without support.
The physiological and behavioral mechanisms linking short sleep to obesity are stronger at younger ages.
“probably because physiological and behavioral mechanisms responsible for this association are stronger in younger ages”
The authors state this as an assumption.
Weight is not gained linearly over the course of a short sleeping period.
“It is possible that weight is not gained linearly over the course of the short sleeping period.”
The paper relies on this without support.
Obesity and obstructive sleep apnea alter leptin and ghrelin regulation and leptin action.
“Obesity is associated with hypoghrelinemia, hyperleptinemia, and leptin resistance, while OSA is associated with hyperghrelinemia, hyperleptinemia, and leptin resistance.”
The paper relies on this without support.
HOMA-IR correlates reasonably well with the glucose clamp and minimal model estimates of insulin sensitivity/resistance.
“HOMA-IR has been found to correlate reasonably well with the glucose clamp and minimal model estimates of insulin sensitivity/resistance in several studies of distinct populations.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“insufficient sleep has been linked to lower energy expenditure, altered glucose homeostasis and alterations in hormones that mediate hunger(24, 25, 27-31).”
From Sleep: important considerations for the prevention of cardiovascular disease (2016) · cites this paper as [24]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Both self-reported short and long sleep duration have been associated with elevated risk of obesity in both children and adults[1-7]”
From Habitual sleep duration associated with self-reported and objectively determined cardiometabolic risk factors (2014) · cites this paper as [4]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Sleep deprivation alters glucose homeostasis, leading to insulin resistance and risk of diabetes(17, 18, 24, 59-61).”
From Sleep: important considerations for the prevention of cardiovascular disease (2016) · cites this paper as [24]
The cited source says what the claim attributes to it.
In the citing paper
“Many studies have found associations between sleep duration and adiposity and obesity.39–41”
From Sleep, Health, and Society (2017) · cites this paper as [40]
The cited source says what the claim attributes to it.
In the citing paper
“diabetes[4, 11, 12]”
From Habitual sleep duration associated with self-reported and objectively determined cardiometabolic risk factors (2014) · cites this paper as [4]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Because the hypothalamic-pituitary-adrenal (HPA) axis regulates a wide range of physiologic processes and is affected by experimental sleep restriction, it is a putative key mediator of the adverse health effects of insufficient sleep (3–11).”
From Adverse effects of two nights of sleep restriction on the hypothalamic-pituitary-adrenal axis in healthy men (2014) · cites this paper as [7]
Experimental — accuracy not yet measuredIn the citing paper
“Because the hypothalamic-pituitary-adrenal (HPA) axis regulates a wide range of physiologic processes and is affected by experimental sleep restriction, it is a putative key mediator of the adverse health effects of insufficient sleep (3–11).”
From Adverse effects of two nights of sleep restriction on the hypothalamic-pituitary-adrenal axis in healthy men (2014) · cites this paper as [7]
In the citing paper
“Habitual short sleep, usually 6 hours or less, has been linked in epidemiological studies to increased mortality and increased prevalence and incidence of numerous pathological conditions including obesity, diabetes, cardiovascular diseases, vulnerability to infection, depression, and anxiety (3–10).”
From Adverse effects of two nights of sleep restriction on the hypothalamic-pituitary-adrenal axis in healthy men (2014) · cites this paper as [7]
In the citing paper
“Because the hypothalamic-pituitary-adrenal (HPA) axis regulates a wide range of physiologic processes and is affected by experimental sleep restriction, it is a putative key mediator of the adverse health effects of insufficient sleep (3–11).”
From Adverse effects of two nights of sleep restriction on the hypothalamic-pituitary-adrenal axis in healthy men (2014) · cites this paper as [7]
In the citing paper
“short sleep duration (6 hours or less), and especially very short sleep duration (less than 5 hours) is associated with increased cardiometabolic morbidity and mortality, including weight gain and obesity, hypertension, hyperlipidemia, and diabetes.”
From Sleep: important considerations for the prevention of cardiovascular disease (2016) · cites this paper as [24]
Citations
Cites
(1992) · Applied Ergonomics · doi:10.1016/0003-6870(92)90318-p · Cited by 5,774
Principles and Practice of Sleep Medicine
Kryger, M. H., Roth, T. G., & Dement, W. C. (2011) · Elsevier eBooks · doi:10.1016/c2009-0-59875-3 · Cited by 5,118
Use and Abuse of HOMA Modeling
Wallace, T. M., Levy, J. C., & Matthews, D. R. (2004) · Diabetes Care · doi:10.2337/diacare.27.6.1487 · Cited by 5,114 · cited 1×
“However, it is a measure of basal insulin sensitivity/resistance and does not provide information about dynamic conditions [201].”
Impact of sleep debt on metabolic and endocrine function
Spiegel, K., Leproult, R., & Van Cauter, E. (1999) · The Lancet · doi:10.1016/s0140-6736(99)01376-8 · Cited by 3,668 · cited 6×
“The two left panels illustrate the effects of reduced sleep duration (adapted from [16, 159]).”
InfluentialSelf-citationDanaei, G., Finucane, M. M., Lu, Y., Singh, G. M., Cowan, M. J., Paciorek, C. J., Lin, J. K., Farzadfar, F., Khang, Y.-H., Stevens, G. A., et al. (2011) · The Lancet · doi:10.1016/s0140-6736(11)60679-x · Cited by 3,568 · cited 1×
“The prevalence of type 2 diabetes is increasing worldwide, reaching pandemic proportions: The number of adults aged 25 years or older with diabetes has more than doubled over nearly three decades and is currently approaching 350 million [34].”
A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans
Cummings, D. E., Purnell, J. Q., Frayo, R. S., Schmidova, K., Wisse, B. E., & Weigle, D. S. (2001) · Diabetes · doi:10.2337/diabetes.50.8.1714 · Cited by 2,940 · cited 1×
“As early as 2001 [32], studies involving frequent sampling across the 24h cycle observed a nocturnal elevation of total ghrelin levels with peak values during the sleep period and declining levels toward the morning.”
Sympathetic neural mechanisms in obstructive sleep apnea.
Somers, V. K., Dyken, M. E., Clary, M. P., & Abboud, F. M. (1995) · Journal of Clinical Investigation · doi:10.1172/jci118235 · Cited by 2,527
Changes in diet and lifestyle and long-term weight gain in women and men
Mozaffarian, D., Hao, T., Rimm, E. B., Willett, W. C., & Hu, F. B. (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1014296 · Cited by 2,527 · cited 1×
“Of the 28 longitudinal studies that examined the impact of short sleep on obesity risk in children and adults, 22 reported that short sleep is associated with an increased risk of weight gain or development of obesity and/or increased fat mass a few years later (reviewed in [80]; additional references: [8, 21, 38, 89,…”
Taheri, S., Lin, L., Austin, D., Young, T., & Mignot, E. (2004) · PLoS Medicine · doi:10.1371/journal.pmed.0010062 · Cited by 2,477 · cited 4×
“These findings are in agreement with the role of leptin in signaling long-term nutritional status, while ghrelin is more involved in acute hunger [174].”
InfluentialSpiegel, K., Tasali, E., Penev, P., & Cauter, E. V. (2004) · Annals of Internal Medicine · doi:10.7326/0003-4819-141-11-200412070-00008 · Cited by 2,459 · cited 10×
“Results regarding subjective feelings of hunger seem less consistent, as only five studies [14, 99, 117, 144, 162] of the 11 [11, 14, 99, 117, 122, 144–146, 162, 170, 194] that examined the effect of reduced sleep duration on hunger reported positive effects.”
InfluentialSelf-citationObesity and the Environment: Where Do We Go from Here?
Hill, J. O., Wyatt, H. R., Reed, G. W., & Peters, J. C. (2003) · Science · doi:10.1126/science.1079857 · Cited by 2,180 · cited 1×
“Such an increase is highly meaningful as the amount of positive energy storage needed to explain the obesity epidemic is ~50 kcal/day [73].”
Kahn, S. E. (2003) · Diabetologia · doi:10.1007/s00125-002-1009-0 · Cited by 2,166 · cited 1×
“Type 2 diabetes is a complex metabolic disorder that involves insulin resistance, impaired insulin secretion, and increased glucose production [37, 79].”
Meta-Analysis of Short Sleep Duration and Obesity in Children and Adults
Cappuccio, F. P., Taggart, F. M., Kandala, N.-B., Currie, A., Peile, E., Stranges, S., & Miller, M. A. (2008) · Sleep · doi:10.1093/sleep/31.5.619 · Cited by 2,076 · cited 5×
“N um be r o f s tu di es 3 [4 2, 7 1, 9 3] 19 [4 , 2 4, 2 6, 2 9– 31 , 5 5, 7 6, 8 8, 1 09 , 1 10 , 1 18 , 1 38 , 1 56 , 1 69 , 1 71 , 1 85 , 1 99 , 2 06 ]”
InfluentialWeight gain as a risk factor for clinical diabetes mellitus in women
Colditz, G. A., Willett, W. C., Rotnitzky, A., & Manson, J. E. (1995) · Annals of Internal Medicine · doi:10.7326/0003-4819-122-7-199504010-00001 · Cited by 2,064 · cited 1×
“However, even modest increases in weight have been shown to have significant implications for long-term adiposity-related metabolic dysfunction, diabetes, cardiovascular disease, and cancer [28, 46, 135, 208].”
Yki-Järvinen, H. (2004) · New England Journal of Medicine · doi:10.1056/nejmra041001 · Cited by 1,830
Quantity and Quality of Sleep and Incidence of Type 2 Diabetes
Cappuccio, F. P., D'Elia, L., Strazzullo, P., & Miller, M. A. (2010) · Diabetes Care · doi:10.2337/dc09-1124 · Cited by 1,670
Guidelines on diabetes, pre-diabetes, and cardiovascular diseases: executive summary
Rydén, L., Standl, E., Bartnik, M., den Berghe, G. V., Betteridge, J. D., de Boer, M., Cosentino, F., Jönsson, B., Laakso, M., Malmberg, K., et al. (2007) · European Heart Journal · doi:10.1093/eurheartj/ehl260 · Cited by 1,644 · cited 1×
“Normal glucose tolerance is achieved when the beta cells are able to secrete appropriate amounts of insulin in a timely manner in combination with adequate hepatic and muscular insulin sensitivity (SI) [137].”
Muniyappa, R., Lee, S., Chen, H., & Quon, M. J. (2008) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00645.2007 · Cited by 1,643 · cited 2×
“Furthermore, it was suggested that the logarithmic transformation of HOMA-IR may be a more appropriate measure for the evaluation of insulin resistance in individuals with glucose intolerance and insulin-resistant conditions [108].”
Short Sleep Duration and Weight Gain: A Systematic Review
Patel, S. R., & Hu, F. B. (2008) · Obesity · doi:10.1038/oby.2007.118 · Cited by 1,505 · cited 2×
“The association between short sleep and increased BMI is particularly strong and consistent in children [82, 100, 124].”
Pathogenesis of type 2 diabetes mellitus
DeFronzo, R. A. (2004) · Medical Clinics of North America · doi:10.1016/j.mcna.2004.04.013 · Cited by 1,342
Obstructive Sleep Apnea Is Independently Associated with Insulin Resistance
Ip, M. S. M., Lam, B., Ng, M. M. T., Lam, W. K., Tsang, K. W. T., & Lam, K. S. L. (2002) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/ajrccm.165.5.2103001 · Cited by 1,300 · cited 1×
“The parameter most consistently found to be positively impacted by CPAP is SI, which is interesting since OSA has been found to be independently associated with insulin resistance [77, 131].”
The neural circuit of orexin (hypocretin): maintaining sleep and wakefulness
Sakurai, T. (2007) · Nature Reviews Neuroscience · doi:10.1038/nrn2092 · Cited by 1,276 · cited 1×
“Orexins (also called hypocretins), two distinct peptides (orexin A and B) synthesized by neurons in the lateral hypothalamus (LH), stimulate not only arousal but also feeding (see [136, 139] for review).”
Lipid-induced insulin resistance: unravelling the mechanism
Samuel, V. T., Petersen, K. F., & Shulman, G. I. (2010) · The Lancet · doi:10.1016/s0140-6736(10)60408-4 · Cited by 1,189 · cited 1×
“Of note, two groups [41, 147] observed that sleep loss was associated with increased levels of free fatty acids, which have been implicated in the pathogenesis of insulin resistance [140].”
Biological, Physiological, Pathophysiological, and Pharmacological Aspects of Ghrelin
van der Lely, A. J., Tschöp, M., Heiman, M. L., & Ghigo, E. (2004) · Endocrine Reviews · doi:10.1210/er.2002-0029 · Cited by 1,187 · cited 2×
“A large body of evidence supports the hypothesis that ghrelin acts on GH secretion, at least in part, via a stimulation of GHRH [39, 50, 192]: A positive interaction between central ghrelinergic activity and sleep, in particular SWS, should therefore be expected.”
Sleep loss: a novel risk factor for insulin resistance and type 2 diabetes
Spiegel, K., Knutson, K., Leproult, R., Tasali, E., & Cauter, E. V. (2005) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00660.2005 · Cited by 1,175
Self-citationPunjabi, N. M. (2004) · American Journal of Epidemiology · doi:10.1093/aje/kwh261 · Cited by 1,107 · cited 1×
“The parameter most consistently found to be positively impacted by CPAP is SI, which is interesting since OSA has been found to be independently associated with insulin resistance [77, 131].”
Thomas, M., Sing, H., Belenky, G., Holcomb, H., Mayberg, H., Dannals, R., Wagner JR., H., Thorne, D., Popp, K., Rowland, L., et al. (2000) · Journal of Sleep Research · doi:10.1046/j.1365-2869.2000.00225.x · Cited by 1,066 · cited 1×
“Considering that the brain is a major user of glucose, the decrease in SG is likely to reflect decreased brain glucose utilization, as shown by PETstudies [183].”
Spiegel, K., Leproult, R., L’Hermite-Balériaux, M., Copinschi, G., Penev, P. D., & Van Cauter, E. (2004) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2004-1003 · Cited by 1,006 · cited 6×
“All found decreased levels of anorexigenic leptin after sleep loss [62, 161, 162].”
InfluentialSelf-citationToward Physiological Understanding of Glucose Tolerance: Minimal-Model Approach
Bergman, R. N. (1989) · Diabetes · doi:10.2337/diab.38.12.1512 · Cited by 1,001 · cited 1×
“After three nights of SWS suppression, SI was decreased by ~25%, reaching the level reported in older adults and in populations at high risk of diabetes [6].”
Weight, Weight Change, and Coronary Heart Disease in Women: Risk Within the 'Normal' Weight Range
Willett, W. C. (1995) · JAMA · doi:10.1001/jama.1995.03520300035033 · Cited by 924
Slow-wave sleep and the risk of type 2 diabetes in humans
Tasali, E., Leproult, R., Ehrmann, D. A., & Van Cauter, E. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0706446105 · Cited by 921 · cited 6×
“Consistent with an increased diabetes risk, glucose tolerance was reduced by ~23% reaching the range typical of older adults with impaired glucose tolerance [176].”
InfluentialAn Instrument to Measure Functional Status Outcomes for Disorders of Excessive Sleepiness
(1997) · Sleep · doi:10.1093/sleep/20.10.835 · Cited by 881 · cited 1×
“Indeed, sleep problems and/or excessive daytime sleepiness significantly reduce physical activity [13, 203].”
Effects of poor and short sleep on glucose metabolism and obesity risk
Spiegel, K., Tasali, E., Leproult, R., & Van Cauter, E. (2009) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2009.23 · Cited by 857 · cited 1×
“The mechanisms through which CPAP may improve glucose metabolism include better sleep quality and continuity and correction of the intermittent hypoxia leading to increased SWS [47, 51, 61, 69, 180], decreased activity of the sympathetic nervous system [111, 157], and decreased weight and/or adiposity through improvem…”
Self-citationExcess weight and sleep-disordered breathing
Young, T., Peppard, P. E., & Taheri, S. (2005) · Journal of Applied Physiology · doi:10.1152/japplphysiol.00587.2005 · Cited by 854 · cited 2×
“suggest that excess weight is responsible for 41–58% of OSA [215].”
Associations between Sleep Loss and Increased Risk of Obesity and Diabetes
Knutson, K. L., & Van Cauter, E. (2008) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1417.033 · Cited by 810 · cited 4×
“Several large cross-sectional studies (reviewed in detail in [82, 178]) have reported an association between short (≤5 or ≤6 h per night) and/or poor sleep and increased prevalence of diabetes or impaired glucose tolerance, after controlling for age, body mass index (BMI), and various other confounders.”
InfluentialIs Sleep Duration Associated With Childhood Obesity? A Systematic Review and Meta‐analysis
Chen, X., Beydoun, M. A., & Wang, Y. (2008) · Obesity · doi:10.1038/oby.2007.63 · Cited by 796 · cited 2×
“These results are in accordance with a meta-analysis of epidemiologic studies that reported a trend for a dose–response relationship between reduced sleep duration and increased risk of obesity [23].”
Leptin Regulation of Neuroendocrine Systems
Ahima, R. S., Saper, C. B., Flier, J. S., & Elmquist, J. K. (2000) · Frontiers in Neuroendocrinology · doi:10.1006/frne.2000.0197 · Cited by 767 · cited 1×
“Leptin inhibits hunger and food intake, increases EE, and promotes fat utilization [1, 193].”
Sleep curtailment is accompanied by increased intake of calories from snacks
Nedeltcheva, A. V., Kilkus, J. M., Imperial, J., Kasza, K., Schoeller, D. A., & Penev, P. D. (2009) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.2008.26574 · Cited by 717 · cited 9×
“Total number of studies 3 [117, 144, 162] 4 [11, 99, 116, 146]”
InfluentialTen Putative Contributors to the Obesity Epidemic
McAllister, E. J., Dhurandhar, N. V., Keith, S. W., Aronne, L. J., Barger, J., Baskin, M., Benca, R. M., Biggio, J., Boggiano, M. M., Eisenmann, J. C., et al. (2009) · Critical Reviews in Food Science and Nutrition · doi:10.1080/10408390903372599 · Cited by 710 · cited 1×
“The extent to which the extended wake resulting from sleep curtailment is spent in activities deleterious for energy homeostasis should also be examined [102].”
Hasler, G., Buysse, D. J., Klaghofer, R., Gamma, A., Ajdacic, V., Eich, D., Rössler, W., & Angst, J. (2004) · Sleep · doi:10.1093/sleep/27.4.661 · Cited by 672 · cited 1×
“To note, one prospective study in adults reported a bidirectional relationship between short sleep and obesity; not only did short sleep predict weight gain a few years later [67], but body weight or obesity also predicted short sleep duration on a later occasion.”
Fos Expression in Orexin Neurons Varies with Behavioral State
Estabrooke, I. V., McCarthy, M. T., Ko, E., Chou, T. C., Chemelli, R. M., Yanagisawa, M., Saper, C. B., & Scammell, T. E. (2001) · The Journal of Neuroscience · doi:10.1523/jneurosci.21-05-01656.2001 · Cited by 654 · cited 1×
“The orexin system has been shown to be overactive when sleep deprivation is behaviorally enforced in rats, dogs, and squirrel monkeys [49, 212, 216], most likely to maintain wakefulness against the increased sleep pressure.”
Adult Weight Change and Risk of Postmenopausal Breast Cancer
Eliassen, A. H., Colditz, G. A., Rosner, B., Willett, W. C., & Hankinson, S. E. (2006) · JAMA · doi:10.1001/jama.296.2.193 · Cited by 654
Roles of Circadian Rhythmicity and Sleep in Human Glucose Regulation
Cauter, E. V., Polonsky, K. S., & Scheen, A. J. (1997) · Endocrine Reviews · doi:10.1210/edrv.18.5.0317 · Cited by 632 · cited 1×
“In addition, changes in counterregulatory hormones and elevated ghrelin levels, which in the next section will be shown to also increase with sleep loss, favor glucose intolerance and hyperinsulinemia [130, 189].”
A Prospective Study of Body Mass Index, Weight Change, and Risk of Stroke in Women
Rexrode, K. M. (1997) · JAMA: The Journal of the American Medical Association · doi:10.1001/jama.1997.03540430051032 · Cited by 617 · cited 1×
“However, even modest increases in weight have been shown to have significant implications for long-term adiposity-related metabolic dysfunction, diabetes, cardiovascular disease, and cancer [28, 46, 135, 208].”
Effects of Sleep Fragmentation on Glucose Metabolism in Normal Subjects
Stamatakis, K. A., & Punjabi, N. M. (2010) · Chest · doi:10.1378/chest.09-0791 · Cited by 614 · cited 5×
“The second study fragmented sleep across all sleep stages during two consecutive nights [167].”
InfluentialRoles of Circadian Rhythmicity and Sleep in Human Glucose Regulation
Van Cauter, E. (1997) · Endocrine Reviews · doi:10.1210/er.18.5.716 · Cited by 608
Sleep Restriction for 1 Week Reduces Insulin Sensitivity in Healthy Men
Buxton, O. M., Pavlova, M., Reid, E. W., Wang, W., Simonson, D. C., & Adler, G. K. (2010) · Diabetes · doi:10.2337/db09-0699 · Cited by 604 · cited 7×
“[16] assessed glucose metabolism by ivGTT and euglycemic– hyperinsulinemic clamp after seven to eight nights of 10-h bedtime and after six to seven nights of 4-h bedtime.”
InfluentialObstructive Sleep Apnea Among Obese Patients With Type 2 Diabetes
Foster, G. D., Sanders, M. H., Millman, R., Zammit, G., Borradaile, K. E., Newman, A. B., Wadden, T. A., Kelley, D., Wing, R. R., Pi Sunyer, F. X., et al. (2009) · Diabetes Care · doi:10.2337/dc08-1776 · Cited by 600 · cited 2×
“, the gold standard method for the diagnosis of OSA, ranged from 58% to 86% [2, 45, 52, 134].”
Harsch, I. A., Schahin, S. P., Radespiel-Tröger, M., Weintz, O., Jahreiß, H., Fuchs, F. S., Wiest, G. H., Hahn, E. G., Lohmann, T., Konturek, P. C., et al. (2004) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.200302-206oc · Cited by 583 · cited 2×
“Methodological differences may also account for the variability of results obtained: four positive studies relied on the hyperinsulinemic–euglycemic clamp technique to assess SI [15, 65, 66, 142], which is considered the gold standard to evaluate SI; another two used continuous glucose monitoring (CGMS) [4, 205], whic…”
Principles and Practice of Sleep Medicine
Awerbuch, G. I. (1990) · Neurology · doi:10.1212/wnl.40.4.731-a · Cited by 579
Cummings, D. E., Frayo, R. S., Marmonier, C., Aubert, R., & Chapelot, D. (2004) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00582.2003 · Cited by 537 · cited 1×
“In humans, ghrelin levels decrease after food ingestion in proportion to caloric load and rise before initiation of the next meal, paralleling the increase in hunger [17, 33].”
Night-To-Night Variability in CPAP Use Over the First Three Months of Treatment
Weaver, T. E., Kribbs, N. B., Pack, A. I., Kline, L. R., Chugh, D. K., Maislin, G., Smith, P. L., Schwartz, A. R., Schubert, N. M., Gillen, K. A., et al. (1997) · Sleep · doi:10.1093/sleep/20.4.278 · Cited by 530
Sleep duration and cardiometabolic risk: A review of the epidemiologic evidence
Knutson, K. L. (2010) · Best Practice & Research Clinical Endocrinology & Metabolism · doi:10.1016/j.beem.2010.07.001 · Cited by 520 · cited 6×
“Nine studies have examined the impact of self-reported sleep duration, and six studies have addressed the impact of sleep quality as determined by selfreport of sleep problems such as difficulty initiating or maintaining sleep or use of sleeping pills (reviewed in [80]).”
InfluentialKolaczynski, J. W., Considine, R. V., Ohannesian, J. P., Marco, C. C., Opentanova, I., Nyce, M. R., Myint, M., & Caro, J. F. (1996) · Diabetes · doi:10.2337/diab.45.11.1511 · Cited by 517 · cited 1×
“Fasting and feeding lowers and elevates leptin levels, respectively [25, 84].”
Diabetes and Sleep Disturbances
Resnick, H. E., Redline, S., Shahar, E., Gilpin, A., Newman, A., Walter, R., Ewy, G. A., Howard, B. V., & Punjabi, N. M. (2003) · Diabetes Care · doi:10.2337/diacare.26.3.702 · Cited by 504 · cited 1×
“, the gold standard method for the diagnosis of OSA, ranged from 58% to 86% [2, 45, 52, 134].”
Chaput, J., Després, J., Bouchard, C., & Tremblay, A. (2007) · Obesity · doi:10.1038/oby.2007.512 · Cited by 498 · cited 1×
“In accordance with most experimental studies conducted in normal weight individuals, the Wisconsin Sleep Cohort Study and the Québec Family Study have shown reduced leptin levels, after controlling for BMI or adiposity, in habitual short sleepers [22, 174].”
St-Onge, M.-P., Roberts, A. L., Chen, J., Kelleman, M., O’Keeffe, M., RoyChoudhury, A., & Jones, P. J. (2011) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.111.013904 · Cited by 463 · cited 6×
“were not related to a comparable rise in energy needs and would, if sustained, eventually result in weight gain [11, 115, 170].”
InfluentialImpact of untreated obstructive sleep apnea on glucose control in type 2 diabetes
Aronsohn, R. S., Whitmore, H., Van Cauter, E., & Tasali, E. (2010) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.200909-1423oc · Cited by 453 · cited 1×
“, the gold standard method for the diagnosis of OSA, ranged from 58% to 86% [2, 45, 52, 134].”
Babu, A. R., Herdegen, J., Fogelfeld, L., Shott, S., & Mazzone, T. (2005) · Archives of Internal Medicine · doi:10.1001/archinte.165.4.447 · Cited by 453 · cited 5×
“Improved glucose tolerance was defined as decreased glucose levels at OGTT , or decreased HbA1c , or lower 24 - h glucose concentrations at CGMS , after CPAP treatment b Improved insulin sensitivity was defined as increased insulin responsiveness index ( M ) or insulin sensitivity index ( ISI ) at HEC , or increased S…”
InfluentialChin, K., Shimizu, K., Nakamura, T., Narai, N., Masuzaki, H., Ogawa, Y., Mishima, M., Nakamura, T., Nakao, K., & Ohi, M. (1999) · Circulation · doi:10.1161/01.cir.100.7.706 · Cited by 450 · cited 1×
“In seven reports, the improved SI resulted in an amelioration of glucose tolerance [4, 24, 68, 71, 118, 169, 205].”
Modulation of glucose regulation and insulin secretion by circadian rhythmicity and sleep
Van Cauter, E., Blackman, J. D., Roland, D., Spire, J. P., Refetoff, S., & Polonsky, K. S. (1991) · Journal of Clinical Investigation · doi:10.1172/jci115396 · Cited by 448 · cited 3×
“Figure 1 shows, from top to bottom, the profiles of GH, cortisol, glucose, and insulin in healthy young men studied during a 53-h period, including 8 h of nocturnal sleep followed by 28 h of continuous wakefulness and 8 h of daytime recovery sleep [151, 152, 187].”
Acute partial sleep deprivation increases food intake in healthy men
Brondel, L., Romer, M. A., Nougues, P. M., Touyarou, P., & Davenne, D. (2010) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.2009.28523 · Cited by 442 · cited 5×
“Results regarding subjective feelings of hunger seem less consistent, as only five studies [14, 99, 117, 144, 162] of the 11 [11, 14, 99, 117, 122, 144–146, 162, 170, 194] that examined the effect of reduced sleep duration on hunger reported positive effects.”
InfluentialIs obesity associated with poor sleep quality in adolescents?
Gupta, N. K., Mueller, W. H., Chan, W., & Meininger, J. C. (2002) · American Journal of Human Biology · doi:10.1002/ajhb.10093 · Cited by 438 · cited 1×
“In support of this hypothesis, four studies that performed objective measurements reported a much stronger cross-sectional association than other studies of similar cross-sectional design but using self-reported data [63, 125, 182, 190].”
Entrainment of the diurnal rhythm of plasma leptin to meal timing.
Schoeller, D. A., Cella, L. K., Sinha, M. K., & Caro, J. F. (1997) · Journal of Clinical Investigation · doi:10.1172/jci119717 · Cited by 433 · cited 1×
“In humans, under normal feeding circumstances, the 24-h leptin profile shows increasing levels during the daytime that culminate in a nocturnal maximum [148].”
Sympathetic nerve activity in obstructive sleep apnoea
Narkiewicz, K., & Somers, V. K. (2003) · Acta Physiologica Scandinavica · doi:10.1046/j.1365-201x.2003.01091.x · Cited by 418 · cited 1×
“The mechanisms through which CPAP may improve glucose metabolism include better sleep quality and continuity and correction of the intermittent hypoxia leading to increased SWS [47, 51, 61, 69, 180], decreased activity of the sympathetic nervous system [111, 157], and decreased weight and/or adiposity through improvem…”
Serum Leptin and Vascular Risk Factors in Obstructive Sleep Apnea
Ip, M., Lam, K. S. L., Ho, C., Tsang, K. W. T., & Lam, W.-K. (2000) · CHEST Journal · doi:10.1378/chest.118.3.580 · Cited by 417
Is sleep duration related to obesity? A critical review of the epidemiological evidence
Marshall, N. S., Glozier, N., & Grunstein, R. R. (2008) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2008.03.001 · Cited by 415 · cited 2×
“The association between short sleep and increased BMI is particularly strong and consistent in children [82, 100, 124].”
West, S. D., Nicoll, D. J., Wallace, T. M., Matthews, D. R., & Stradling, J. R. (2007) · Thorax · doi:10.1136/thx.2006.074351 · Cited by 408 · cited 1×
“One study reporting unchanged SI in type 2 diabetes patients after therapeutic CPAP also included a group of patients who underwent sham CPAP [206]; in this study, the patients underwent a hyperinsulinemic–euglycemic clamp, the gold standard for evaluation of SI, but the average nightly therapeutic CPAP use was only 3.”
Xiang, A. H., Peters, R. K., Kjos, S. L., Marroquin, A., Goico, J., Ochoa, C., Kawakubo, M., & Buchanan, T. A. (2006) · Diabetes · doi:10.2337/diabetes.55.02.06.db05-1066 · Cited by 402 · cited 1×
“Furthermore, three of the 11 subjects had DI values <1000, indicating a high risk of diabetes [213].”
Schmid, S. M., Hallschmid, M., Jauch-Chara, K., Wilms, B., Benedict, C., Lehnert, H., Born, J., & Schultes, B. (2009) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.2009.27984 · Cited by 400 · cited 9×
“Total number of studies 3 [117, 144, 162] 4 [11, 99, 116, 146]”
InfluentialInsufficient Sleep Undermines Dietary Efforts to Reduce Adiposity
Nedeltcheva, A. V., Kilkus, J. M., Imperial, J., Schoeller, D. A., & Penev, P. D. (2010) · Annals of Internal Medicine · doi:10.7326/0003-4819-153-7-201010050-00006 · Cited by 397 · cited 10×
“Results regarding subjective feelings of hunger seem less consistent, as only five studies [14, 99, 117, 144, 162] of the 11 [11, 14, 99, 117, 122, 144–146, 162, 170, 194] that examined the effect of reduced sleep duration on hunger reported positive effects.”
InfluentialDonga, E., van Dijk, M., van Dijk, J. G., Biermasz, N. R., Lammers, G.-J., van Kralingen, K. W., Corssmit, E. P. M., & Romijn, J. A. (2010) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2009-2430 · Cited by 387 · cited 3×
“Of note, two groups [41, 147] observed that sleep loss was associated with increased levels of free fatty acids, which have been implicated in the pathogenesis of insulin resistance [140].”
Obstructive Sleep Apnea and Type 2 Diabetes
Tasali, E., Mokhlesi, B., & Van Cauter, E. (2008) · Chest · doi:10.1378/chest.07-0828 · Cited by 371 · cited 1×
“It is now well-documented that OSA, independently of age, sex, BMI, and other confounders, is associated with glucose intolerance, insulin resistance, and diabetes (for review, see [175, 177]).”
SCHMID, S. M., HALLSCHMID, M., JAUCH‐CHARA, K., BORN, J., & SCHULTES, B. (2008) · Journal of Sleep Research · doi:10.1111/j.1365-2869.2008.00662.x · Cited by 370 · cited 9×
“Results regarding subjective feelings of hunger seem less consistent, as only five studies [14, 99, 117, 144, 162] of the 11 [11, 14, 99, 117, 122, 144–146, 162, 170, 194] that examined the effect of reduced sleep duration on hunger reported positive effects.”
InfluentialObstructive sleep apnea and type 2 diabetes
Rasche, K., Keller, T., Tautz, B., Hader, C., Hergenç, G., Antosiewicz, J., Giulio, C. D., & Pokorski, M. (2010) · European journal of medical research · doi:10.1186/2047-783x-15-s2-152 · Cited by 367
Obstructive Sleep Apnea and Metabolic Syndrome: Alterations in Glucose Metabolism and Inflammation
Tasali, E., & Ip, M. S. M. (2008) · Proceedings of the American Thoracic Society · doi:10.1513/pats.200708-139mg · Cited by 365 · cited 1×
“It is now well-documented that OSA, independently of age, sex, BMI, and other confounders, is associated with glucose intolerance, insulin resistance, and diabetes (for review, see [175, 177]).”
Rimonabant as an adjunct therapy in overweight/obese patients with type 2 diabetes: reply
Rydén, L., & Standl, E. (2007) · European Heart Journal · doi:10.1093/eurheartj/ehm124 · Cited by 365
Lyssenko, V., Almgren, P., Anevski, D., Perfekt, R., Lahti, K., Nissén, M., Isomaa, B., Forsen, B., Homström, N., Saloranta, C., et al. (2005) · Diabetes · doi:10.2337/diabetes.54.1.166 · Cited by 362 · cited 1×
“The disposition index (DI), the product of AIRg and SI, which provides an estimate of beta-cell function relative to the prevailing level of insulin resistance, has been shown to be a validated marker of diabetes risk [96, 123].”
Longitudinal associations between sleep duration and subsequent weight gain: A systematic review
Magee, L., & Hale, L. (2012) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2011.05.005 · Cited by 355 · cited 1×
“As a consequence, “in order for short sleep to predict any physiological or behavioral change, the longitudinal time frame examined would need to start prior to or at the beginning of the short sleep transition for each participant” [98], which is less likely to be the case with older ages.”
Nielsen, L. S., Danielsen, K. V., & Sørensen, T. I. A. (2011) · Obesity Reviews · doi:10.1111/j.1467-789x.2010.00724.x · Cited by 338 · cited 1×
“However, this may be the consequence, at least in part, of measurements errors since both sleep and weight assessments were based on self-reports in nearly all epidemiologic studies [119].”
Nedeltcheva, A. V., Kessler, L., Imperial, J., & Penev, P. D. (2009) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2009-0483 · Cited by 323 · cited 6×
“were not related to a comparable rise in energy needs and would, if sustained, eventually result in weight gain [11, 115, 170].”
InfluentialCallahan, H. S., Cummings, D. E., PEPE, M. S., Breen, P. A., Matthys, C. C., & Weigle, D. S. (2004) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2003-031267 · Cited by 321 · cited 1×
“In humans, ghrelin levels decrease after food ingestion in proportion to caloric load and rise before initiation of the next meal, paralleling the increase in hunger [17, 33].”
Jung, C. M., Melanson, E. L., Frydendall, E. J., Perreault, L., Eckel, R. H., & Wright, K. P. (2011) · The Journal of Physiology · doi:10.1113/jphysiol.2010.197517 · Cited by 318 · cited 3×
“Although it is well established that EE is lower during sleep [10, 53, 78, 207], relatively few studies have evaluated the impact of sleep loss on daytime and/or 24 h EE.”
Cardiovascular and metabolic effects of CPAP in obese males with OSA
Coughlin, S. R., Mawdsley, L., Mugarza, J. A., Wilding, J. P. H., & Calverley, P. M. (2007) · European Respiratory Journal · doi:10.1183/09031936.00043306 · Cited by 313 · cited 1×
“sham CPAP in obese OSA patients [30].”
Bodosi, B., Gardi, J., Hajdu, I., Szentirmai, É., Obál, F., & Krueger, J. M. (2004) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00294.2004 · Cited by 305 · cited 1×
“An inhibitory influence of sleep deprivation would contradict animal studies linking the promotion of feeding with the maintenance of wakefulness [9, 172, 173].”
Sleep and Brain Energy Levels: ATP Changes during Sleep
Dworak, M., McCarley, R. W., Kim, T., Kalinchuk, A. V., & Basheer, R. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.1423-10.2010 · Cited by 297 · cited 1×
“A recently published study in rats [43] reported an increase in ATP levels in wake-active brain regions at the beginning of the sleep period, in tight association with SWA.”
Brooks, B. (1994) · Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.79.6.1681 · Cited by 295 · cited 1×
“Methodological differences may also account for the variability of results obtained: four positive studies relied on the hyperinsulinemic–euglycemic clamp technique to assess SI [15, 65, 66, 142], which is considered the gold standard to evaluate SI; another two used continuous glucose monitoring (CGMS) [4, 205], whic…”
Dorková, Z., Petrášová, D., Molčányiová, A., Popovnakova, M., & Tkáčová, R. (2008) · CHEST Journal · doi:10.1378/chest.08-0556 · Cited by 286 · cited 1×
“Furthermore, two studies reported lower fasting glucose and insulin levels in CPAP treated patients [42, 71], while one observed improved fasting glucose concentrations but unchanged fasting insulin levels [142].”
The association between sleep duration and obesity in older adults
Groups, F. T. O. F. I. M. A. T. S. O. O. F. R., Patel, S. R., Blackwell, T., Redline, S., Ancoli-Israel, S., Cauley, J. A., Hillier, T. A., Lewis, C. E., Orwoll, E. S., Stefanick, M. L., et al. (2008) · International Journal of Obesity · doi:10.1038/ijo.2008.198 · Cited by 284 · cited 1×
“In support of this hypothesis, four studies that performed objective measurements reported a much stronger cross-sectional association than other studies of similar cross-sectional design but using self-reported data [63, 125, 182, 190].”
Watanabe, M., Kikuchi, H., Tanaka, K., & Takahashi, M. (2010) · Sleep · doi:10.1093/sleep/33.2.161 · Cited by 263 · cited 2×
“Of the 28 longitudinal studies that examined the impact of short sleep on obesity risk in children and adults, 22 reported that short sleep is associated with an increased risk of weight gain or development of obesity and/or increased fat mass a few years later (reviewed in [80]; additional references: [8, 21, 38, 89,…”
Sleep Loss Reduces Diurnal Rhythm Amplitude of Leptin in Healthy Men
Mullington, J. M., Chan, J. L., Van Dongen, H. P. A., Szuba, M. P., Samaras, J., Price, N. J., Meier‐Ewert, H. K., Dinges, D. F., & Mantzoros, C. S. (2003) · Journal of Neuroendocrinology · doi:10.1046/j.1365-2826.2003.01069.x · Cited by 261 · cited 1×
“The stimulating impact of sleep on leptin has also been evidenced in a subsequent study that showed decreased amplitude of the leptin diurnal variation during prolonged total sleep deprivation [107].”
Relationship between sleepiness and general health status
Briones, B., Adams, N., Strauss, M., Rosenberg, C., Whalen, C., Carskadon, M., Roebuck, T., Winters, M., & Redline, S. (1996) · SLEEP · doi:10.1093/sleep/19.7.583 · Cited by 253 · cited 1×
“Indeed, sleep problems and/or excessive daytime sleepiness significantly reduce physical activity [13, 203].”
Sleep deprivation in the rat by the disk-over-water method
Rechtschaffen, A., & Bergmann, B. M. (1995) · Behavioural Brain Research · doi:10.1016/0166-4328(95)00020-t · Cited by 253 · cited 1×
“In rodents, food shortage or starvation results in decreased sleep [35], and, conversely, total sleep deprivation leads to marked hyperphagia [133].”
Liu, J., Prudom, C. E., Nass, R., Pezzoli, S. S., Oliveri, M. C., Johnson, M. L., Veldhuis, P., Gordon, D. A., Howard, A. D., Witcher, D. R., et al. (2008) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2007-2235 · Cited by 248 · cited 1×
“All [95, 166] but one [3] of the studies that have attempted to characterize the overnight profiles of acylated ghrelin in relation to unacylated ghrelin confirmed the increased nocturnal elevation in total ghrelin and demonstrated a concomitant increase in acylated ghrelin.”
Acute sleep deprivation reduces energy expenditure in healthy men
Benedict, C., Hallschmid, M., Lassen, A., Mahnke, C., Schultes, B., Schiöth, H. B., Born, J., & Lange, T. (2011) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.110.006460 · Cited by 243 · cited 8×
“, after 72–126 h of TSD [86] and after 24 h of TSD [5].”
InfluentialChildhood Sleep Time and Long-Term Risk for Obesity: A 32-Year Prospective Birth Cohort Study
Landhuis, C. E., Poulton, R., Welch, D., & Hancox, R. J. (2008) · Pediatrics · doi:10.1542/peds.2007-3521 · Cited by 237 · cited 2×
“This pattern is particularly consistent in pediatric populations (all 12 studies had positive findings; reviewed in [80]; additional references: [21, 38, 89, 150]).”
Simon, C., Gronfier, C., Schlienger, J. L., & Brandenberger, G. (1998) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.83.6.4864 · Cited by 236
Impact of acute sleep restriction on cortisol and leptin levels in young women
Omisade, A., Buxton, O. M., & Rusak, B. (2010) · Physiology & Behavior · doi:10.1016/j.physbeh.2010.01.028 · Cited by 235 · cited 6×
“[122], bedtimes were restricted to 3 h for only 1 day, and leptin levels were measured only at 2 time points during daytime.”
InfluentialPrevalence of Sleep Apnea in a Population of Adults with Type 2 Diabetes Mellitus
Einhorn, D., Stewart, D. A., Erman, M. K., Gordon, N., Philis-Tsimikas, A., & Casal, E. (2007) · Endocrine Practice · doi:10.4158/ep.13.4.355 · Cited by 232 · cited 1×
“, the gold standard method for the diagnosis of OSA, ranged from 58% to 86% [2, 45, 52, 134].”
Longitudinal analysis of sleep in relation to BMI and body fat in children: the FLAME study
Carter, P. J., Taylor, B. J., Williams, S. M., & Taylor, R. W. (2011) · BMJ · doi:10.1136/bmj.d2712 · Cited by 226 · cited 3×
“only pediatric prospective study that obtained concomitant objective measurements of sleep, weight, and body composition demonstrated that the increased weight gain in children sleeping less was the result of selective increased fat deposition [21].”
Plat, L., Leproult, R., L’Hermite-Baleriaux, M., Fery, F., Mockel, J., Polonsky, K. S., & Van Cauter, E. (1999) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.84.9.5978 · Cited by 225 · cited 1×
“In addition, changes in counterregulatory hormones and elevated ghrelin levels, which in the next section will be shown to also increase with sleep loss, favor glucose intolerance and hyperinsulinemia [130, 189].”
Short sleep duration and obesity: the role of emotional stress and sleep disturbances
Vgontzas, A. N., Lin, H.-M., Papaliaga, M., Calhoun, S., Vela-Bueno, A., Chrousos, G. P., & Bixler, E. O. (2008) · International Journal of Obesity · doi:10.1038/ijo.2008.4 · Cited by 224 · cited 1×
“In addition, a large scale study [198] concluded that self-reported short sleep in obese adults may be a surrogate marker of subjective sleep disturbance [196].”
Influence of Partial Sleep Deprivation on Energy Balance and Insulin Sensitivity in Healthy Women
Bosy-Westphal, A., Hinrichs, S., Jauch-Chara, K., Hitze, B., Later, W., Wilms, B., Settler, U., Peters, A., Kiosz, D., & Müller, M. J. (2008) · Obesity Facts · doi:10.1159/000158874 · Cited by 221 · cited 10×
“[11] are the only group who focused exclusively on pre-menopausal women, who may be more resistant to the alterations in glucose metabolism induced by sleep deprivation.”
InfluentialHarsch, I. A., Schahin, S. P., Brückner, K., Radespiel-Tröger, M., Fuchs, F. S., Hahn, E. G., Konturek, P. C., Lohmann, T., & Ficker, J. H. (2004) · Respiration · doi:10.1159/000077423 · Cited by 219 · cited 1×
“Methodological differences may also account for the variability of results obtained: four positive studies relied on the hyperinsulinemic–euglycemic clamp technique to assess SI [15, 65, 66, 142], which is considered the gold standard to evaluate SI; another two used continuous glucose monitoring (CGMS) [4, 205], whic…”
Minimal Model: Perspective from 2005
Bergman, R. N. (2005) · Hormone Research in Paediatrics · doi:10.1159/000089312 · Cited by 216
Lilly lecture 1989. Toward physiological understanding of glucose tolerance. Minimal-model approach
Bergman, R. N. (1989) · Diabetes · doi:10.2337/diabetes.38.12.1512 · Cited by 215
Abstracts of the IDF Congress in Paris 2003
(2003) · Diabetologia · doi:10.1007/s00125-003-1190-9 · Cited by 211
Van Cauter, E. (1992) · Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.74.6.1441 · Cited by 205 · cited 1×
“In fact, in healthy young men, a major GH pulse that accounts for roughly 70% of the daily production occurs shortly after sleep onset [188], in association with the first phase of slow wave sleep (SWS).”
Altered sleep regulation in leptin-deficient mice
Laposky, A. D., Shelton, J., Bass, J., Dugovic, C., Perrino, N., & Turek, F. W. (2006) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00304.2005 · Cited by 203 · cited 1×
“The relationship between leptin and sleep appears to be bidirectional; systemic administration of leptin to normally fed rats increases SWS and decreases REM sleep [155], and leptin deficiency in ob/ob mice disrupts sleep architecture and impairs sleep consolidation [90].”
Boyle, P. J., Scott, J. C., Krentz, A. J., Nagy, R. J., Comstock, E., & Hoffman, C. (1994) · Journal of Clinical Investigation · doi:10.1172/jci117003 · Cited by 202 · cited 1×
“SWS, which is particularly abundant at the beginning of the sleep period, has been shown to result in a 30–40% decrease in cerebral glucose metabolism relative to waking or rapid eye movement (REM) sleep [12].”
Effects of a growth hormone pulse on total and forearm substrate fluxes in humans
Moller, N., Jorgensen, J. O., Schmitz, O., Moller, J., Christiansen, J., Alberti, K. G., & Orskov, H. (1990) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1990.258.1.e86 · Cited by 194 · cited 1×
“Muscle relaxation and the rapid hyperglycemic effects of the sleeponset GH pulse account for the remaining fall in glucose uptake during early sleep [103].”
van den Berg, J. F., Knvistingh Neven, A., Tulen, J. H. M., Hofman, A., Witteman, J. C. M., Miedema, H. M. E., & Tiemeier, H. (2008) · International Journal of Obesity · doi:10.1038/ijo.2008.57 · Cited by 193 · cited 1×
“In support of this hypothesis, four studies that performed objective measurements reported a much stronger cross-sectional association than other studies of similar cross-sectional design but using self-reported data [63, 125, 182, 190].”
Sleep enhances nocturnal plasma ghrelin levels in healthy subjects
Dzaja, A., Dalal, M. A., Himmerich, H., Uhr, M., Pollmächer, T., & Schuld, A. (2004) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00527.2003 · Cited by 184 · cited 1×
“Only two studies directly examined the role of sleep on nocturnal ghrelin release in humans: one found that sleep deprivation inhibited total ghrelin levels [44]; the other study found that sleep deprivation inhibited total ghrelin at the beginning of the night and stimulated total ghrelin in the second half of the ni…”
Adaptation of the 24-h growth hormone profile to a state of sleep debt
Spiegel, K., Leproult, R., Colecchia, E. F., L'Hermite-Balériaux, M., Nie, Z., Copinschi, G., & Van Cauter, E. (2000) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.2000.279.3.r874 · Cited by 183 · cited 2×
“Increased evening cortisol concentrations, extended duration of elevated GH concentrations during the waking period, and increased cardiac sympathovagal balance were also observed in the sleep loss condition [159–161], all of which could underlie the clinically significant deleterious impact of recurrent sleep restric…”
Self-citationNatalucci, G., Riedl, S., Gleiss, A., Zidek, T., & Frisch, H. (2005) · European Journal of Endocrinology · doi:10.1530/eje.1.01919 · Cited by 182 · cited 1×
“In addition to its orexigenic effects, ghrelin has also been identified as a potent GH secretagogue based on exogenous administration [56], and a correlation between GH and ghrelin levels has been reported in some, but not all, studies [3, 48, 85, 106, 112, 113, 149].”
Plat, L. (1999) · Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.84.9.3082 · Cited by 177
Metabolic rate and breathing during sleep
White, D. P., Weil, J. V., & Zwillich, C. W. (1985) · Journal of Applied Physiology · doi:10.1152/jappl.1985.59.2.384 · Cited by 176 · cited 2×
“Although it is well established that EE is lower during sleep [10, 53, 78, 207], relatively few studies have evaluated the impact of sleep loss on daytime and/or 24 h EE.”
Lam, J. C. M., Lam, B., Yao, T. J., Lai, A. Y. K., Ooi, C. G., Tam, S., Lam, K. S. L., & Ip, M. S. M. (2010) · European Respiratory Journal · doi:10.1183/09031936.00047709 · Cited by 170 · cited 1×
“In 12 of these, an improvement in SI was reported after as little as 2 days of CPAP treatment in non-obese patients [65] and 1 week in obese patients [88].”
Williams, C. J., Hu, F. B., Patel, S. R., & Mantzoros, C. S. (2007) · Diabetes Care · doi:10.2337/dc06-2107 · Cited by 168
Dependence of sleep on nutrients' availability
Danguir, J., & Nicolaidis, S. (1979) · Physiology & Behavior · doi:10.1016/0031-9384(79)90240-3 · Cited by 164
Espelund, U. S., Hansen, T. K., Højlund, K., Beck‐Nielsen, H., Clausen, J. T., Hansen, B. S., Ørskov, H., Jørgensen, J. O. L., & Frystyk, J. (2005) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2004-0604 · Cited by 157 · cited 1×
“In addition to its orexigenic effects, ghrelin has also been identified as a potent GH secretagogue based on exogenous administration [56], and a correlation between GH and ghrelin levels has been reported in some, but not all, studies [3, 48, 85, 106, 112, 113, 149].”
Ghrelin drives GH secretion during fasting in man
Muller, A., Lamberts, S., Janssen, J. A. M. J. L., Hofland, L. J., van Koetsveld, P. M., Bidlingmaier, M., Strasburger, C., Ghigo, E., & van der Lely, A. (2002) · European Journal of Endocrinology · doi:10.1530/eje.0.1460203 · Cited by 156 · cited 1×
“In addition to its orexigenic effects, ghrelin has also been identified as a potent GH secretagogue based on exogenous administration [56], and a correlation between GH and ghrelin levels has been reported in some, but not all, studies [3, 48, 85, 106, 112, 113, 149].”
Metabolism during normal, fragmented, and recovery sleep
Bonnet, M. H., Berry, R. B., & Arand, D. L. (1991) · Journal of Applied Physiology · doi:10.1152/jappl.1991.71.3.1112 · Cited by 153 · cited 2×
“Although it is well established that EE is lower during sleep [10, 53, 78, 207], relatively few studies have evaluated the impact of sleep loss on daytime and/or 24 h EE.”
Short Sleep Duration and Body Mass Index: A Prospective Longitudinal Study in Preadolescence
Seegers, V., Petit, D., Falissard, B., Vitaro, F., Tremblay, R. E., Montplaisir, J., & Touchette, E. (2011) · American Journal of Epidemiology · doi:10.1093/aje/kwq389 · Cited by 153 · cited 2×
“This pattern is particularly consistent in pediatric populations (all 12 studies had positive findings; reviewed in [80]; additional references: [21, 38, 89, 150]).”
CPAP treatment of a population-based sample—what are the benefits and the treatment compliance?
Lindberg, E., Berne, C., Elmasry, A., Hedner, J. A., & Janson, C. (2006) · Sleep Medicine · doi:10.1016/j.sleep.2005.12.010 · Cited by 151 · cited 1×
“Finally, a population-based study involving 28 OSA patients and 28 controls matched for age, smoking status, and comorbidities found a significant decrease only in fasting insulin levels, after 3 weeks of CPAP treatment, while the decrease in SI, assessed by HOMA-IR, failed to reach statistical significance [93].”
SIMON, C., BRANDENBERGER, G., & FOLLENIUS, M. (1987) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-64-4-669 · Cited by 147 · cited 3×
“Figure 1 shows, from top to bottom, the profiles of GH, cortisol, glucose, and insulin in healthy young men studied during a 53-h period, including 8 h of nocturnal sleep followed by 28 h of continuous wakefulness and 8 h of daytime recovery sleep [151, 152, 187].”
Wu, M.-F., John, J., Maidment, N. T., Lam, H. A., & Siegel, J. M. (2002) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00207.2002 · Cited by 146 · cited 1×
“The orexin system has been shown to be overactive when sleep deprivation is behaviorally enforced in rats, dogs, and squirrel monkeys [49, 212, 216], most likely to maintain wakefulness against the increased sleep pressure.”
Hassaballa, H. A., Tulaimat, A., Herdegen, J. J., & Mokhlesi, B. (2005) · Sleep And Breathing · doi:10.1007/s11325-005-0033-y · Cited by 142 · cited 2×
“In seven reports, the improved SI resulted in an amelioration of glucose tolerance [4, 24, 68, 71, 118, 169, 205].”
Disturbed Glucoregulatory Response to Food Intake After Moderate Sleep Restriction
Schmid, S. M., Hallschmid, M., Jauch-Chara, K., Wilms, B., Lehnert, H., Born, J., & Schultes, B. (2011) · Sleep · doi:10.1093/sleep/34.3.371 · Cited by 140 · cited 7×
“The same authors [147] later reported a decreased glucagon response to an ad libitum breakfast compared to the rested condition, suggesting again a reduced function of the pancreatic alpha cells.”
InfluentialSteiger, A. (2003) · Journal of Internal Medicine · doi:10.1046/j.1365-2796.2003.01175.x · Cited by 137 · cited 3×
“Taken together, these results indicate that sleep–wake homeostasis is a major determinant of GH secretion [59, 168, 186].”
Effects of morning cortisol elevation on insulin secretion and glucose regulation in humans
Plat, L., Byrne, M. M., Sturis, J., Polonsky, K. S., Mockel, J., Fery, F., & Van Cauter, E. (1996) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1996.270.1.e36 · Cited by 132 · cited 1×
“This progressive increase in glucose uptake is likely to reflect the replacement of SWS by REM sleep and the increased insulin sensitivity due to a delayed effect of low cortisol levels during the evening and early part of the night [129].”
Guilleminault, C., Kim, Y., Chowdhuri, S., Horita, M., Ohayon, M., & Kushida, C. (2001) · European Respiratory Journal · doi:10.1183/09031936.01.17508380 · Cited by 132 · cited 19×
“The first study selectively suppressed SWS in healthy young adults during three consecutive nights [ 176 ] .”
InfluentialHenley, D., Russell, G. M., Douthwaite, J. A., Wood, S. A., Buchanan, F., Gibson, R. H., Woltersdorf, W. W. W., Catterall, J. R., & Lightman, S. L. (2009) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2009-1174 · Cited by 129 · cited 1×
“However, two studies involving frequent (q30 and q10 min) blood sampling over a 24-h period observed a decrease in cortisol and ACTH levels in OSA patients following treatment [72, 197].”
Reduced Sleep Duration or Quality: Relationships With Insulin Resistance and Type 2 Diabetes
Tasali, E., Leproult, R., & Spiegel, K. (2009) · Progress in Cardiovascular Diseases · doi:10.1016/j.pcad.2008.10.002 · Cited by 129 · cited 3×
“5 h in bed [178], and middle-aged obese subjects submitted to four to five nights of restriction or extension of their habitual sleep schedule by 2–3 h/night ate 15% more calories in the bedtime restriction condition [104].”
Self-citationVgontzas, A. N., Pejovic, S., Zoumakis, E., Lin, H. ‐., Bentley, C. M., Bixler, E. O., Sarrigiannidis, A., Basta, M., & Chrousos, G. P. (2007) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2007-0774 · Cited by 129 · cited 1×
“However, two studies involving frequent (q30 and q10 min) blood sampling over a 24-h period observed a decrease in cortisol and ACTH levels in OSA patients following treatment [72, 197].”
Comondore, V. R., Cheema, R., Fox, J. M., Butt, A., Mancini, G. B. J., Fleetham, J. A., Ryan, C. F., Chan, S., & Ayas, N. (2008) · Lung · doi:10.1007/s00408-008-9115-5 · Cited by 128
PEJOVIC, S., VGONTZAS, A. N., BASTA, M., TSAOUSSOGLOU, M., ZOUMAKIS, E., VGONTZAS, A., BIXLER, E. O., & CHROUSOS, G. P. (2010) · Journal of Sleep Research · doi:10.1111/j.1365-2869.2010.00844.x · Cited by 127 · cited 1×
“Conversely, no impact of TSD was evidenced in another recent study that also reported reduced amplitude of the 24-h leptin diurnal variation due to increased daytime leptin levels [126].”
Tasali, E., Chapotot, F., Leproult, R., Whitmore, H. R., & Ehrmann, D. A. (2010) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2010-1187 · Cited by 127 · cited 21×
“The first study selectively suppressed SWS in healthy young adults during three consecutive nights [ 176 ] .”
InfluentialEffect of sleep deprivation on insulin sensitivity and cortisol concentration in healthy subjects.
González-Ortı́z, M., Martínez‐Abundis, E., Balcázar-Muñoz, B. R., & Pascoe-González, S. (2000) · PubMed · Cited by 125
Ghrelin microinjection into forebrain sites induces wakefulness and feeding in rats
Szentirmai, É., Kapás, L., & Krueger, J. M. (2006) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00448.2006 · Cited by 125 · cited 1×
“An inhibitory influence of sleep deprivation would contradict animal studies linking the promotion of feeding with the maintenance of wakefulness [9, 172, 173].”
The effects of leptin on REM sleep and slow wave deltain rats are reversed by food deprivation
Sinton, C. M., Fitch, T. E., & Gershenfeld, H. K. (1999) · Journal of Sleep Research · doi:10.1046/j.1365-2869.1999.00158.x · Cited by 122 · cited 1×
“The relationship between leptin and sleep appears to be bidirectional; systemic administration of leptin to normally fed rats increases SWS and decreases REM sleep [155], and leptin deficiency in ob/ob mice disrupts sleep architecture and impairs sleep consolidation [90].”
The selfish brain: Competition for energy resources
Peters, A. (2010) · American Journal of Human Biology · doi:10.1002/ajhb.21106 · Cited by 121 · cited 1×
“The brain consumes up to two thirds of the circulating glucose [127].”
Effects of sleep deprivation and exercise on glucose tolerance.
VanHelder, T., Symons, J. D., & Radomski, M. W. (1993) · PubMed · Cited by 119
Selective effects of CPAP on sleep apnoea‐associated manifestations
Vgontzas, A. N., Zoumakis, E., Bixler, E. O., Lin, H., Collins, B., Basta, M., Pejovic, S., & Chrousos, G. P. (2008) · European Journal of Clinical Investigation · doi:10.1111/j.1365-2362.2008.01984.x · Cited by 118
CPAP treatment does not affect glucose–insulin metabolism in sleep apneic patients
Smurra, M. V., Philip, P., Taillard, J., Guilleminault, C., Bioulac, B. H., & Gin, H. (2001) · Sleep Medicine · doi:10.1016/s1389-9457(00)00079-4 · Cited by 116
Çuhadaroğlu, Ç., Utkusavaş, A., Öztürk, L., Salman, S., & Ece, T. (2009) · Lung · doi:10.1007/s00408-008-9131-5 · Cited by 116 · cited 1×
“Out of four studies that evaluated beta-cell function [31, 71, 109, 180], only one [31] observed an improvement in this parameter, as assessed by the homeostatic model assessment (HOMA-beta); somewhat surprisingly, all other markers of glucose homeostasis (fasting glucose and insulin levels, HOMA-IR) were unchanged by…”
Schmid, S. M., Hallschmid, M., Jauch-Chara, K., Bandorf, N., Born, J., & Schultes, B. (2007) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2006-2788 · Cited by 115 · cited 19×
“Total sleep deprivation studies Very few studies have evaluated the impact of TSD on subsequent levels of hormones involved in appetite regulation and subjective feelings of hunger .”
InfluentialKolaczynski, J. W., Considine, R. V., Ohannesian, J., et al. (1996) · Diabetes · doi:10.2337/diabetes.45.11.1511 · Cited by 111
Treatment of obesity with extension of sleep duration: a randomized, prospective, controlled trial
Cizza, G., Marincola, P., Mattingly, M., Williams, L., Mitler, M. M., Skarulis, M. C., & Csákó, G. (2010) · Clinical Trials · doi:10.1177/1740774510368298 · Cited by 110 · cited 1×
“Such a study is currently under progress [27].”
Efficacy and Reliability of the Continuous Glucose Monitoring System
Gross, T. M., & Mastrototaro, J. J. (2000) · Diabetes Technology & Therapeutics · doi:10.1089/15209150050214087 · Cited by 108 · cited 1×
“Methodological differences may also account for the variability of results obtained: four positive studies relied on the hyperinsulinemic–euglycemic clamp technique to assess SI [15, 65, 66, 142], which is considered the gold standard to evaluate SI; another two used continuous glucose monitoring (CGMS) [4, 205], whic…”
Simpson, N. S., Banks, S., & Dinges, D. F. (2010) · Biological Research For Nursing · doi:10.1177/1099800410366301 · Cited by 108 · cited 3×
“Twelve studies assessed the impact of partial sleep deprivation on leptin and ghrelin [11, 62, 99, 116, 117, 122, 144, 146, 154, 161, 162, 194].”
Spiegel, K., Tasali, E., Leproult, R., Scherberg, N., & Van Cauter, E. (2011) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2010-1978 · Cited by 106 · cited 2×
“All [95, 166] but one [3] of the studies that have attempted to characterize the overnight profiles of acylated ghrelin in relation to unacylated ghrelin confirmed the increased nocturnal elevation in total ghrelin and demonstrated a concomitant increase in acylated ghrelin.”
Self-citationPhysiology, stress, and malnutrition : functional correlates, nutritional intervention
Kinney, J. M., & Tucker, H. N. (1997) · Medical Entomology and Zoology · Cited by 104
Prolonged Sleep Restriction Affects Glucose Metabolism in Healthy Young Men
van Leeuwen, W. M. A., Hublin, C., Sallinen, M., Härmä, M., Hirvonen, A., & Porkka-Heiskanen, T. (2010) · International Journal of Endocrinology · doi:10.1155/2010/108641 · Cited by 102 · cited 7×
“Two other studies [41, 194] reported only a decrease in SI, with apparent preservation of glucose tolerance.”
InfluentialAssociations between Short Sleep Duration and Central Obesity in Women
Theorell-Haglöw, J., Berne, C., Janson, C., Sahlin, C., & Lindberg, E. (2010) · Sleep · doi:10.1093/sleep/33.5.593 · Cited by 102 · cited 1×
“In support of this hypothesis, four studies that performed objective measurements reported a much stronger cross-sectional association than other studies of similar cross-sectional design but using self-reported data [63, 125, 182, 190].”
Heinzer, R. C., Gaudreau, H., Décary, A., Sforza, E. A., Petit, D., Morisson, F., & Montplaisir, J. Y. (2001) · CHEST Journal · doi:10.1378/chest.119.6.1807 · Cited by 101 · cited 19×
“The first study selectively suppressed SWS in healthy young adults during three consecutive nights [ 176 ] .”
InfluentialTrenell, M. I., Ward, J. A., Yee, B. J., Phillips, C. L., Kemp, G. J., Grunstein, R. R., & Thompson, C. H. (2006) · Diabetes Obesity and Metabolism · doi:10.1111/j.1463-1326.2006.00649.x · Cited by 98
Unraveling the role of the ghrelin gene peptides in the endocrine pancreas
Granata, R., Baragli, A., Settanni, F., Scarlatti, F., & Ghigo, E. (2010) · Journal of Molecular Endocrinology · doi:10.1677/jme-10-0019 · Cited by 97 · cited 1×
“In contrast to leptin, ghrelin stimulates hunger and food intake, reduces EE, and promotes the retention of fat [56, 58, 92, 191].”
Associations between short sleep duration and central obesity in women.
Theorell‐Haglöw, J., Berne, C., Janson, C., Sahlin, C., & Lindberg, E. (2010) · Europe PMC (PubMed Central) · Cited by 95
Preliminary observations on the effects of sleep time in a sleep restriction paradigm
Guilleminault, C., Powell, N. B., Martinez, S., Kushida, C., Raffray, T., Palombini, L., & Philip, P. (2003) · Sleep Medicine · doi:10.1016/s1389-9457(03)00061-3 · Cited by 93 · cited 4×
“All found decreased levels of anorexigenic leptin after sleep loss [62, 161, 162].”
InfluentialEvidence for Acyl-Ghrelin Modulation of Growth Hormone Release in the Fed State
Nass, R. M., Farhy, L. S., Liu, J., Prudom, C. E., Johnson, M. L., Veldhuis, P. P., Pezzoli, S. S., Oliveri, M. C., Gaylinn, B. D., Geysen, H. M., et al. (2008) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2007-2234 · Cited by 90 · cited 1×
“In addition to its orexigenic effects, ghrelin has also been identified as a potent GH secretagogue based on exogenous administration [56], and a correlation between GH and ghrelin levels has been reported in some, but not all, studies [3, 48, 85, 106, 112, 113, 149].”
Package Unit Size and Amount of Food: Do Both Influence Intake?
Raynor, H. A., & Wing, R. R. (2007) · Obesity · doi:10.1038/oby.2007.274 · Cited by 89 · cited 2×
“Consistent with the fact that overeating usually occurs when unlimited palatable food is available [132], the subjects overate and gained ~2 kg in each sleep condition [116].”
Littman, A. J., Vitiello, M. V., Foster-Schubert, K., Ulrich, C. M., Tworoger, S. S., Potter, J. D., Weigle, D. S., & McTiernan, A. (2007) · International Journal of Obesity · doi:10.1038/sj.ijo.0803438 · Cited by 86 · cited 2×
“Of the 28 longitudinal studies that examined the impact of short sleep on obesity risk in children and adults, 22 reported that short sleep is associated with an increased risk of weight gain or development of obesity and/or increased fat mass a few years later (reviewed in [80]; additional references: [8, 21, 38, 89,…”
Weight, Weight Change, and Coronary Heart Disease in Women
&NA; (1996) · Journal of Occupational and Environmental Medicine · doi:10.1097/00043764-199605000-00003 · Cited by 86
Effect of nasal CPAP treatment on insulin sensitivity and plasma leptin
Saarelainen, S., Lahtela, J. T., & Kallonen, E. (1997) · Journal of Sleep Research · doi:10.1046/j.1365-2869.1997.00034.x · Cited by 85
Ghrelin-induced sleep responses in ad libitum fed and food-restricted rats
Szentirmai, É., Hajdu, I., Obál, F., & Krueger, J. M. (2006) · Brain Research · doi:10.1016/j.brainres.2006.02.072 · Cited by 84 · cited 1×
“An inhibitory influence of sleep deprivation would contradict animal studies linking the promotion of feeding with the maintenance of wakefulness [9, 172, 173].”
Role of endogenous ghrelin in growth hormone secretion, appetite regulation and metabolism
Dimaraki, E. V., & Jaffe, C. A. (2007) · Reviews in Endocrine and Metabolic Disorders · doi:10.1007/s11154-006-9022-0 · Cited by 84 · cited 2×
“A large body of evidence supports the hypothesis that ghrelin acts on GH secretion, at least in part, via a stimulation of GHRH [39, 50, 192]: A positive interaction between central ghrelinergic activity and sleep, in particular SWS, should therefore be expected.”
LYYTIKÄINEN, P., RAHKONEN, O., LAHELMA, E., & LALLUKKA, T. (2011) · Journal of Sleep Research · doi:10.1111/j.1365-2869.2010.00903.x · Cited by 81 · cited 2×
“Of the 28 longitudinal studies that examined the impact of short sleep on obesity risk in children and adults, 22 reported that short sleep is associated with an increased risk of weight gain or development of obesity and/or increased fat mass a few years later (reviewed in [80]; additional references: [8, 21, 38, 89,…”
Nakra, N., Bhargava, S., Dzuira, J. D., Caprio, S., & Bazzy‐Asaad, A. (2008) · PEDIATRICS · doi:10.1542/peds.2008-0154 · Cited by 81 · cited 1×
“One group [110] focused on children with metabolic syndrome and sleep-disordered breathing treated with CPAP for 12 months and observed no improvement in glucose tolerance or SI; however, the compliance to CPAP is not reported.”
Accelerated ribosome formation and growth in neonatal pig hearts
Camacho, J. A., Peterson, C. J., White, G. J., & Morgan, H. E. (1990) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.1990.258.1.c86 · Cited by 81
Sørensen, T. I. A. (2009) · Proceedings of the Nutrition Society · doi:10.1017/s0029665108008847 · Cited by 75 · cited 1×
“Such phenomenon is observed for other weight promoting behaviors, notably physical inactivity and overeating, both of which are reinforced by weight gain [158].”
The Role of Leptin in the Regulation of Energy Balance and Adiposity
Van Dijk, G. (2001) · Journal of Neuroendocrinology · doi:10.1046/j.1365-2826.2001.00707.x · Cited by 75 · cited 1×
“Leptin inhibits hunger and food intake, increases EE, and promotes fat utilization [1, 193].”
Weight and metabolic effects of cpap in obstructive sleep apnea patients with obesity
Garcia, J. M., Sharafkhaneh, H., Hirshkowitz, M., Elkhatib, R., & Sharafkhaneh, A. (2011) · Respiratory Research · doi:10.1186/1465-9921-12-80 · Cited by 75
Tomfohr‐Madsen, L. M., Edwards, K. M., & Dimsdale, J. E. (2012) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2011.05.003 · Cited by 72 · cited 1×
“The effect of CPAP on the activity of the hypothalamic–pituitary–adrenal axis is still debated [184].”
Chin-Chance, C. (2000) · Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.85.8.2685 · Cited by 69 · cited 3×
“As leptin levels are enhanced by food intake and correlate with the degree of obesity [25], these latter results may be the expected consequence of the positive energy balance achieved by increased food intake [11, 116, 146] and weight gain [11,”
Endogenous Circulating Ghrelin Does Not Mediate Growth Hormone Rhythmicity or Response to Fasting
Avram, A. M., Jaffe, C. A., Symons, K. V., & Barkan, A. L. (2005) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2004-1785 · Cited by 67 · cited 2×
“All [95, 166] but one [3] of the studies that have attempted to characterize the overnight profiles of acylated ghrelin in relation to unacylated ghrelin confirmed the increased nocturnal elevation in total ghrelin and demonstrated a concomitant increase in acylated ghrelin.”
Steiropoulos, P., Παπάνας, Ν., Nena, E., Tsara, V., Fitili, C., Τzouvelekis, Α., Christaki, P. I., Maltezos, E. S., & Bouros, D. E. (2009) · Sleep Medicine · doi:10.1016/j.sleep.2008.10.004 · Cited by 67 · cited 1×
“In seven reports, the improved SI resulted in an amelioration of glucose tolerance [4, 24, 68, 71, 118, 169, 205].”
Schahin, S. P., Nechanitzky, T., Dittel, C., Fuchs, F. S., Hahn, E. G., Konturek, P. C., Ficker, J. H., & Harsch, I. A. (2008) · PubMed · Cited by 66
Obesity and short sleep: unlikely bedfellows?
Horne, J. A. (2011) · Obesity Reviews · doi:10.1111/j.1467-789x.2010.00847.x · Cited by 63 · cited 1×
“Critics have questioned the relevance of this link by putting forward the weakness of the association [74].”
Ultradian rhythms in pituitary and adrenal hormones: their relations to sleep
Gronfier, C., & Brandenberger, G. (1998) · Sleep Medicine Reviews · doi:10.1016/s1087-0792(98)90051-x · Cited by 63 · cited 3×
“Taken together, these results indicate that sleep–wake homeostasis is a major determinant of GH secretion [59, 168, 186].”
Bo, S., Ciccone, G., Durazzo, M., Ghinamo, L., Villois, P., Canil, S., Gambino, R., Cassader, M., Gentile, L., & Cavallo-Perin, P. (2011) · International Journal of Obesity · doi:10.1038/ijo.2011.5 · Cited by 61 · cited 1×
“Of the 28 longitudinal studies that examined the impact of short sleep on obesity risk in children and adults, 22 reported that short sleep is associated with an increased risk of weight gain or development of obesity and/or increased fat mass a few years later (reviewed in [80]; additional references: [8, 21, 38, 89,…”
Petrie, J. R., Pearson, E. R., & Sutherland, C. D. (2010) · Biochemical Pharmacology · doi:10.1016/j.bcp.2010.11.010 · Cited by 61 · cited 1×
“Recent genome-wide association studies have identified genetic loci that predispose to glucose intolerance [128].”
Vesico-ureteric reflux and urinary tract development in the Pax21Neu+/−mouse
Murawski, I. J., Myburgh, D. B., Favor, J., & Gupta, I. R. (2007) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00221.2007 · Cited by 61
Effect of sleep and circadian cycle on sleep period energy expenditure
Fraser, G., Trinder, J., Colrain, I. M., & Montgomery, I. (1989) · Journal of Applied Physiology · doi:10.1152/jappl.1989.66.2.830 · Cited by 61 · cited 2×
“Although it is well established that EE is lower during sleep [10, 53, 78, 207], relatively few studies have evaluated the impact of sleep loss on daytime and/or 24 h EE.”
Carneiro, G., Togeiro, S. M., Ribeiro‐Filho, F. F., Truksinas, E., Ribeiro, A. B., Zanella, M. T., & Tufik, S. (2009) · Metabolic Syndrome and Related Disorders · doi:10.1089/met.2009.0019 · Cited by 59
Nishiura, C., & Hashimoto, H. (2010) · Journal of Epidemiology · doi:10.2188/jea.je20100019 · Cited by 59 · cited 1×
“Of the 28 longitudinal studies that examined the impact of short sleep on obesity risk in children and adults, 22 reported that short sleep is associated with an increased risk of weight gain or development of obesity and/or increased fat mass a few years later (reviewed in [80]; additional references: [8, 21, 38, 89,…”
(1969) · PubMed · Cited by 58
de Lima, A. M. J., Franco, C. M. R., de Castro, C. M. M. B., Bezerra, A. D. A., Ataíde, L., & Halpern, A. (2009) · Respiration · doi:10.1159/000227800 · Cited by 56 · cited 2×
“Another group [36] included data about both obese non-OSA controls and non-compliant OSA patients (<4 h CPAP use per night), and observed improvement in SI, assessed by the homeostatic model assessment (HOMA-IR), only in the patients with good treatment adherence.”
Nocturnal ghrelin pulsatility and response to growth hormone secretagogues in healthy men
Koutkia, P., Hron, B. M., Breu, J. J., Johnson, M. L., & Grinspoon, S. K. (2004) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00548.2003 · Cited by 56 · cited 1×
“In addition to its orexigenic effects, ghrelin has also been identified as a potent GH secretagogue based on exogenous administration [56], and a correlation between GH and ghrelin levels has been reported in some, but not all, studies [3, 48, 85, 106, 112, 113, 149].”
Mild Sleep Restriction Acutely Reduces Plasma Glucagon Levels in Healthy Men
Schmid, S. M., Jauch-Chara, K., Hallschmid, M., & Schultes, B. (2009) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2009-0969 · Cited by 55 · cited 5×
“Number of studies 7 [16, 41, 91, 115, 147, 159, 194] 3 [11, 145, 217]”
InfluentialEffects of sleep-deprivation on the activity of selected metabolic enzymes in skeletal-muscle
Vondra, K., Brodan, V., Bass, A., Kuhn, E., Teisinger, J., AndĚl, M., & Veselková, A. (1981) · European Journal of Applied Physiology and Occupational Physiology · doi:10.1007/bf00422481 · Cited by 53 · cited 18×
“Total sleep deprivation studies Very few studies have evaluated the impact of TSD on subsequent levels of hormones involved in appetite regulation and subjective feelings of hunger .”
InfluentialSchuessler, P., Uhr, M., Ising, M., Schmid, D. A., WEIKEL, J., & Steiger, A. (2005) · Journal of Sleep Research · doi:10.1111/j.1365-2869.2005.00486.x · Cited by 52 · cited 1×
“In addition to its orexigenic effects, ghrelin has also been identified as a potent GH secretagogue based on exogenous administration [56], and a correlation between GH and ghrelin levels has been reported in some, but not all, studies [3, 48, 85, 106, 112, 113, 149].”
Fietze, I., Quispe-Bravo, S., HÄNSCH, T., Röttig, J., & WITT, G. B. C. (1997) · Journal of Sleep Research · doi:10.1046/j.1365-2869.1997.00029.x · Cited by 51 · cited 19×
“The first study selectively suppressed SWS in healthy young adults during three consecutive nights [ 176 ] .”
InfluentialSimon, C., Brandenberger, G., Saini, J., Ehrhart, J., & Follenius, M. (1994) · Sleep · doi:10.1093/sleep/17.4.333 · Cited by 49 · cited 3×
“Figure 1 shows, from top to bottom, the profiles of GH, cortisol, glucose, and insulin in healthy young men studied during a 53-h period, including 8 h of nocturnal sleep followed by 28 h of continuous wakefulness and 8 h of daytime recovery sleep [151, 152, 187].”
Diethelm, K., Bolzenius, K., Cheng, G., Remer, T., & Buyken, A. E. (2011) · International Journal of Pediatric Obesity · doi:10.3109/17477166.2011.566338 · Cited by 48
Wehrens, S. M. T., Hampton, S. M., Finn, R. E., & Skene, D. J. (2010) · Journal of Endocrinology · doi:10.1677/joe-10-0077 · Cited by 47 · cited 20×
“Total sleep deprivation studies Very few studies have evaluated the impact of TSD on subsequent levels of hormones involved in appetite regulation and subjective feelings of hunger .”
InfluentialNo effect of 8‐week time in bed restriction on glucose tolerance in older long sleepers
ZIELINSKI, M. R., KLINE, C. E., KRIPKE, D. F., BOGAN, R. K., & YOUNGSTEDT, S. D. (2008) · Journal of Sleep Research · doi:10.1111/j.1365-2869.2008.00673.x · Cited by 44 · cited 5×
“[217] assessed the effect of semi-chronic (8 weeks) sleep curtailment on glucose tolerance in self-reported older long sleepers (≥8.”
InfluentialChung, S., Yoon, I., Lee, C. H., & Kim, J. (2010) · Sleep And Breathing · doi:10.1007/s11325-009-0323-x · Cited by 42
Murri, M., Alcázar-Ramírez, J., Garrido‐Sánchez, L., Linde, F., Alcaide, J., Cardona, F., & Tinahones, F. J. (2009) · Translational research · doi:10.1016/j.trsl.2009.06.001 · Cited by 42 · cited 1×
“Out of four studies that evaluated beta-cell function [31, 71, 109, 180], only one [31] observed an improvement in this parameter, as assessed by the homeostatic model assessment (HOMA-beta); somewhat surprisingly, all other markers of glucose homeostasis (fasting glucose and insulin levels, HOMA-IR) were unchanged by…”
Acute sleep restriction alters neuroendocrine hormones and appetite in healthy male adults
MAGEE, C. A., HUANG, X.-F., IVERSON, D. C., & CAPUTI, P. (2009) · Sleep and Biological Rhythms · doi:10.1111/j.1479-8425.2009.00396.x · Cited by 42 · cited 9×
“Results regarding subjective feelings of hunger seem less consistent, as only five studies [14, 99, 117, 144, 162] of the 11 [11, 14, 99, 117, 122, 144–146, 162, 170, 194] that examined the effect of reduced sleep duration on hunger reported positive effects.”
Influential
Research works printed but not linked: 1
- Spiegel K et al (2005) The 24-hour profile of plasma PYY levels in normal adults: relationships with sleep, meal intake and ghrelin levels. In: The Endocrine Society’s 87th Annual Meeting Abstract number OR8-3, San Diego, CA, USA, June 2005, pp. 82–83
Cited by
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The effects of physical activity on sleep: A meta-analytic review
Kredlow, M. A., Capozzoli, M. C., Hearon, B. A., Calkins, A. W., & Otto, M. W. (2015) · Journal of Behavioral Medicine · doi:10.1007/s10865-015-9617-6 · Cited by 1,333
“…temperature changes (McGinty & Szymusiak, 1990), cytokine concentration changes (Santos et al., 2007), increased energy consumption/metabolic rate (Morselli et al., 2012), CNS fatigue (Uchida et al., 2012), changes in mood/anxiety symptoms (Buman & King, 2010; Uchida et al., 2012), changes in…”
BackgroundSt-Onge, M.-P., Grandner, M. A., Brown, D., Conroy, M. B., Jean-Louis, G., Coons, M., & Bhatt, D. L. (2016) · Circulation · doi:10.1161/cir.0000000000000444 · Cited by 1,044
Sleep and exercise: A reciprocal issue?
Chennaoui, M., Arnal, P. J., Sauvet, F., & Léger, D. (2014) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2014.06.008 · Cited by 770
Grandner, M. A. (2017) · Sleep Medicine Clinics · doi:10.1016/j.jsmc.2016.10.012 · Cited by 720
Fatima, Y., Doi, S. A. R., & Mamun, A. A. (2015) · Obesity Reviews · doi:10.1111/obr.12245 · Cited by 577
Metadata
- Authors
- Morselli, L. L., Guyon, A., & Spiegel, K.
- Affiliations
- University of Chicago (US)
- Lyon 1 Université (FR)
- Corresponding author
- Spiegel, Karine
- Venue
- Pflügers Archiv - European Journal of Physiology
- Published
- 2011-11-19
- Volume
- 463
- Issue
- 1
- Pages
- 139-160
- ISSN
- 0031-6768 (ISSN-L)
- 1432-2013
- PMC
- PMC3289068
- OpenAlex
- W1966891298
- Semantic Scholar
- 28ae604abbcdd449c303e162c78fe2dd56e66a64
- Cited by
- 199
- References
- 230
- Citations by year
- 2026: 8 · 2025: 13 · 2024: 9 · 2023: 11 · 2022: 13 · 2021: 15 · 2020: 13 · 2019: 10 · 2018: 6 · 2017: 10 · 2016: 24 · 2015: 21 · 2014: 23 · 2013: 10 · 2012: 12
- FWCI
- 1.91
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Pflügers Archiv - European Journal of Physiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Funders
- National Institute on Aging (P01-AG11412., P01AG011412)
- National Heart, Lung, and Blood Institute (R01HL075079, R01HL075025)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK-071960, P60DK20595, P60DK020595)
- National Center for Research Resources (M01RR000055)
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Health Sciences › Medicine › Physiology (medical) › Obstructive Sleep Apnea Research
- Keywords
- sleep, metabolic function, glucose homeostasis, appetite regulation, sleep duration, sleep quality, obesity, diabetes mellitus, obstructive sleep apnea, intermittent hypoxemia, continuous positive airway pressure, endocrine function
- MeSH terms
- Animals, Appetite Regulation, Diabetes Mellitus, Glucose, Humans, Metabolism, Obesity, Sleep, Sleep Apnea, Obstructive
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-09, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-09 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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