The DOI matches its Crossref record; 227 of the 230 references it cites were found in a registry or an index; 4 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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Written from the paper’s full text.
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
107 Not checked yet · 18 Own interpretation · 7 No basis given · 2 Partly supported · 1 Supported · 1 Supported so far · 1 Own result · accuracy not yet measured
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
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Supported
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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)
plaindirect- 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
boostedcorrelational- 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
plaindirect- 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
plaindirect- 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
plaincorrelational- 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
plaindirect- 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
“As shown in Fig. 1b, this profile is only modestly affected by the presence or absence of sleep.”
§ 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
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“As early as 2001 [32], studies involving frequent sampling across the 24-h cycle observed a nocturnal elevation of total ghrelin levels with peak values during the sleep period and declining levels toward the morning.”
§ 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 [32] Cummings DE et al (2001) A preprandial rise in plasma ghrelin levels suggests a role in meal initiation in humans. Diabetes 50:1714–1719 source
plaincorrelational- 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
“Of these seven studies, six reported a deleterious impact of TSD on at least one aspect of glucose metabolism.”
§ Sleep and metabolic function > Short sleep and/or poor sleep loss as risk factors of diabetes > Evidence from experimental laboratory studies
plaindirect- Asserted: passes — The authors put it forward as true.
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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)
plaindirect- Asserted: passes — The authors put it forward as true.
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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)
plaindirect- 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
plaincorrelational- 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
plaindirect- 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
hedgedcorrelational- 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
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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
plaindirect- Asserted: passes — The authors put it forward as true.
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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
plaindirectn = 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
plaincorrelational- Asserted: passes — The authors put it forward as true.
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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
plaindirect- 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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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
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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
hedgedcorrelational- 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
plaincorrelational- 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
“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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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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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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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
plainconditional- 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
plaincorrelational- 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.
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
hedgedconditional- 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
“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
plaindirect- 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
“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
plaindirect- 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: 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
plaindirect- 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
“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
plaindirect- 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
hedgeddirect- 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
“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
hedgedcorrelational- 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
boostedcorrelational- 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
plaincorrelational- 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
hedgedconditional- 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
plaindirect- 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
“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
hedgeddirect- 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
hedgedconditional- 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
“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
hedgedconditional- 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
hedgedconditional- 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
hedgedconditional- 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
plaindirect- 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
hedgeddirect- 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
plaindirect- 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
hedgedconditional- 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
plaindirect- 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
plaindirect- 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
plaincorrelational- 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
“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 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]
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]
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]
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]
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]
Citations
Cites
Items 201–227 of 227
Ghrelin and New Metabolic Frontiers
van der Lely, A. J. (2009) · Hormone Research in Paediatrics · doi:10.1159/000178055 · Cited by 42 · cited 3×
“While ghrelin acylation, under the control of the enzyme ghrelin-O-acyl-transferase (GOAT), is essential for its orexigenic effects [92, 191], most of the physiology of human ghrelin has been based on the measurement of blood levels of total ghrelin, which mainly reflect unacylated ghrelin levels.”
Feng, D. D., Yang, S.-K., Loudes, C., Simon, A., Al-Sarraf, T., Culler, M., Alvear-Perez, R., Llorens-Cortes, C., Chen, C., Epelbaum, J., et al. (2011) · European Journal of Neuroscience · doi:10.1111/j.1460-9568.2011.07787.x · Cited by 41 · 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 and metabolism: Role of hypothalamic neuronal circuitry
Rolls, A., Borg, J. S., & de Lecea, L. (2010) · Best Practice & Research Clinical Endocrinology & Metabolism · doi:10.1016/j.beem.2010.08.002 · Cited by 39 · 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).”
No Association Between Leptin Levels and Sleep Duration or Quality in Obese Adults
Knutson, K. L., Galli, G., Zhao, X., Mattingly, M., Cizza, G., & Study, ;. F. T. N. S. E. (2011) · Obesity · doi:10.1038/oby.2011.248 · Cited by 38 · cited 1×
“In contrast to these two studies that enrolled men and women of various body composition (lean, overweight, and obese), three subsequent studies did not confirm the link between sleep duration, leptin and ghrelin levels: One involved only overweight postmenopausal women [94], another one only women mostly overweight o…”
Short Sleep and Obesity: Are Poor Sleep, Chronic Stress, and Unhealthy Behaviors the Link?
Vgontzas, A. N., & Bixler, E. O. (2008) · SLEEP · doi:10.5665/sleep/31.9.1203 · Cited by 36 · 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].”
Henley, D., Buchanan, F., Gibson, R. H., Douthwaite, J. A., Wood, S. A., Woltersdorf, W. W. W., Catterall, J. R., & Lightman, S. L. (2009) · Journal of Endocrinology · doi:10.1677/joe-09-0245 · Cited by 36 · cited 3×
“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].”
Genetic Mapping of Disposition Index and Acute Insulin Response Loci on Chromosome 11q
Palmer, N. D., Langefeld, C. D., Campbell, J. K., Williams, A. H., Saad, M. F., Norris, J. M., Haffner, S. M., Rotter, J. I., Wagenknecht, L. E., Bergman, R. N., et al. (2006) · Diabetes · doi:10.2337/diabetes.55.04.06.db05-0813 · Cited by 36 · 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].”
Glucose Metabolism in Older Adults: A Study Including Subjects More Than 80 Years of Age
Garcia, G. V., Freeman, R. V., Supiano, M. A., Smith, M. J., Galecki, A. T., & Halter, J. B. (1997) · Journal of the American Geriatrics Society · doi:10.1111/j.1532-5415.1997.tb01507.x · Cited by 35 · cited 1×
“the subjects were in a state of sleep debt and reached values typical for older adults with impaired glucose tolerance [54].”
Ghrelin’s Role as a Major Regulator of Appetite and Its Other Functions in Neuroendocrinology
Lim, C. T., Kola, B., Korbonits, M., & Grossman, A. B. (2010) · Progress in Brain Research · doi:10.1016/s0079-6123(10)82008-4 · Cited by 34 · cited 2×
“While ghrelin acylation, under the control of the enzyme ghrelin-O-acyl-transferase (GOAT), is essential for its orexigenic effects [92, 191], most of the physiology of human ghrelin has been based on the measurement of blood levels of total ghrelin, which mainly reflect unacylated ghrelin levels.”
Stoohs, R. A., Facchini, F. S., Philip, P., Valencia‐Flores, M., & Guilleminault, C. (1993) · SLEEP · doi:10.1093/sleep/16.suppl_8.s141 · Cited by 34
Zeitzer, J. M., Buckmaster, C. L., Lyons, D. M., & Mignot, E. (2007) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00460.2007 · Cited by 31 · 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.”
Endocrine and Metabolic Actions of Ghrelin
Gasco, V., Beccuti, G., Marotta, F., Benso, A., Granata, R., Broglio, F., & Ghigo, E. (2010) · Endocrine Development · doi:10.1159/000262531 · Cited by 30 · cited 2×
“In contrast to leptin, ghrelin stimulates hunger and food intake, reduces EE, and promotes the retention of fat [56, 58, 92, 191].”
Oktay, B. K., Akbal, E., Fırat, H., Ardıç, S., & Kızılgün, M. (2009) · Acta Clinica Belgica · doi:10.1179/acb.2009.051 · Cited by 29
Nena, E., Steiropoulos, P., Τzouvelekis, Α., Tsara, V., Hatzizisi, O., Kyriazis, G., Froudarakis, Μ. E., Trakada, G., Παπάνας, Ν., & Bouros, D. E. (2010) · Respiration · doi:10.1159/000295903 · Cited by 25 · cited 1×
“In seven reports, the improved SI resulted in an amelioration of glucose tolerance [4, 24, 68, 71, 118, 169, 205].”
Changes in sleep duration and changes in weight in obese patients: The Swedish Obese Subjects Study
MARSHALL, N. S., GRUNSTEIN, R. R., PELTONEN, M., STENLOF, K., HEDNER, J., & SJOSTROM, L. V. (2010) · Sleep and Biological Rhythms · doi:10.1111/j.1479-8425.2010.00431.x · Cited by 17 · 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,…”
Lee-Chiong, T. L., & Polnitsky, C. A. (2007) · Elsevier eBooks · doi:10.1016/b978-075067563-5.10004-5 · Cited by 15
Kumor, M., Bielicki, P., Przybyłowski, T., Rubinsztajn, R., Zielinski, J., & Chazan, R. (2011) · Advances in respiratory medicine · doi:10.5603/arm.27655 · Cited by 13
What is the Meaning of the ATP Surge During Sleep?
Wong‐Riley, M. T. T. (2011) · SLEEP · doi:10.5665/sleep.1102 · Cited by 10 · cited 1×
“Although these results have been challenged by other authors [64, 70, 210, 211], they are in line with earlier reports of decreased brain energy use during non-REM (NREM) sleep.”
nCPAP Treatment of Obstructive Sleep Apnea Increases Slow Wave Sleep in Prefrontal EEG
Eskelinen, V., Uibu, T., & Himanen, S. (2007) · Clinical EEG and Neuroscience · doi:10.1177/155005940703800311 · Cited by 10 · cited 19×
“The first study selectively suppressed SWS in healthy young adults during three consecutive nights [ 176 ] .”
InfluentialApples to oranges: comparing long sleep to short sleep
Knutson, K. L., & Leproult, R. (2010) · Journal of Sleep Research · doi:10.1111/j.1365-2869.2009.00770.x · Cited by 9 · cited 1×
“Furthermore, sleep duration was also decreased in the control group, and the final difference in total sleep time between the two groups was only approximately 16 min [81].”
Cardiovascular and metabolic effects of CPAP in obese obstructive sleep apnoea patients: Table 1—
Teramoto, S., Yamaguchi, Y., Yamamoto, H., et al. (2007) · European Respiratory Journal · doi:10.1183/09031936.00105707 · Cited by 8
Repeatability Is Not the Same as Accuracy
Heller, H. C. (2011) · SLEEP · doi:10.5665/sleep.1108 · Cited by 8 · cited 1×
“Although these results have been challenged by other authors [64, 70, 210, 211], they are in line with earlier reports of decreased brain energy use during non-REM (NREM) sleep.”
Does the Brain Gain Back Energy During Sleep? But What Does It Mean?
Haddad, G. G. (2011) · SLEEP · doi:10.5665/sleep.1104 · Cited by 7 · cited 1×
“Although these results have been challenged by other authors [64, 70, 210, 211], they are in line with earlier reports of decreased brain energy use during non-REM (NREM) sleep.”
Wei, C.-Y., Wang, H., Li, J., et al. (2009) · PubMed · Cited by 7
Measuring In Vivo Metabolite Levels in Brain
Wilson, D. F. (2011) · SLEEP · doi:10.5665/sleep.1106 · Cited by 6 · cited 1×
“Although these results have been challenged by other authors [64, 70, 210, 211], they are in line with earlier reports of decreased brain energy use during non-REM (NREM) sleep.”
M-J-089 IMPACT OF SLEEP RESTRICTION ON THE REGULATION OF APPETITE IN MIDDLE-AGED OBESE SUBJECTS
Morselli, L. L., Balbo, M., Van Cauter, E., Guyon, A., & Spiegel, K. (2011) · Sleep Medicine · doi:10.1016/s1389-9457(11)70169-1 · Cited by 5 · cited 2×
“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-citationLeproult, R., & Cauter, E. V. (2006) · Dépôt institutionnel de l'Université libre de Bruxelles (Université Libre de Bruxelles) · Cited by 2
Research works printed but not linked: 1
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Cited by
Sorted by citations
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
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