The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index; 25 of the 44 sources its claims cite were checked for support.
Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction: A Randomized, Crossover Study
Open accessAbstract
BACKGROUND: Insufficient sleep increases the risk for insulin resistance, type 2 diabetes, and obesity, suggesting that sleep restriction may impair peripheral metabolic pathways. Yet, a direct link between sleep restriction and alterations in molecular metabolic pathways in any peripheral human tissue has not been shown. OBJECTIVE: To determine whether sleep restriction results in reduced insulin sensitivity in subcutaneous fat, a peripheral tissue that plays a pivotal role in energy metabolism and balance. DESIGN: Randomized, 2-period, 2-condition, crossover clinical study. SETTING: University of Chicago Clinical Resource Center. PARTICIPANTS: Seven healthy adults (1 woman, 6 men) with a mean age of 23.7 years (SD, 3.8) and mean body mass index of 22.8 kg/m(2) (SD, 1.6). INTERVENTION: Four days of 4.5 hours in bed or 8.5 hours in bed under controlled conditions of caloric intake and physical activity. MEASUREMENTS: Adipocytes collected from subcutaneous fat biopsy samples after normal and restricted sleep conditions were exposed to incremental insulin concentrations. The ability of insulin to increase levels of phosphorylated Akt (pAkt), a crucial step in the insulin-signaling pathway, was assessed. Total Akt (tAkt) served as a loading control. The insulin concentration for the half-maximal stimulation of the pAkt-tAkt ratio was used as a measure of cellular insulin sensitivity. Total body insulin sensitivity was assessed using a frequently sampled intravenous glucose tolerance test. RESULTS: The insulin concentration for the half-maximal pAkt-tAkt response was nearly 3-fold higher (mean, 0.71 nM [SD, 0.27] vs. 0.24 nM [SD, 0.24]; P = 0.01; mean difference, 0.47 nM [SD, 0.33]; P = 0.01), and the total area under the receiver-operating characteristic curve of the pAkt-tAkt response was 30% lower (P = 0.01) during sleep restriction than during normal sleep. A reduction in total body insulin sensitivity (P = 0.02) paralleled this impaired cellular insulin sensitivity. LIMITATION: This was a single-center study with a small sample size. CONCLUSION: Sleep restriction results in an insulin-resistant state in human adipocytes. Sleep may be an important regulator of energy metabolism in peripheral tissues. PRIMARY FUNDING SOURCE: National Institutes of Health.
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Claims the paper makes
12 Own method · 7 Own interpretation · 6 Own result · 3 Partly supported · 2 Supported so far · 2 Mixed support · 1 Couldn’t confirm · 1 No full text of the sources · 1 Not checked yet · accuracy not yet measured
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“well-controlled laboratory studies in healthy adults have shown that repeated partial sleep restriction has adverse effects on systemic insulin sensitivity and glucose tolerance”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Abstract > Primary Funding Source
What the sources say
- Disputedcites [11] sourceExperimental — accuracy not yet measured
The Results section (‘Impact of Sleep Loss on Insulin Sensitivity and Glucose Tolerance’) reports that insulin sensitivity and the response to an oral glucose load remained unchanged after four nights of sleep curtailment. The Discussion (p. 272) likewise says this short-term intervention in healthy women had no effect on basal or post-OGTT glucose metabolism, while leaving open possible long-term effects. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
- Supportedcites [12] source
The Discussion (passages 4–5; page numbers not supplied) reports that one week of restricted sleep significantly reduced insulin sensitivity in healthy men. It also reports an earlier laboratory study in healthy subjects that found reduced glucose tolerance after repeated sleep restriction. Together, these support the citing sentence’s broad statement. (LLM, conf=0.90)
- Partly supportedcites [13] sourceExperimental — accuracy not yet measured
The Abstract reports that repeated partial sleep restriction impairs glucose tolerance, but says its effects on insulin sensitivity had not been characterized. The Discussion reports reduced insulin sensitivity after a single night of restriction in healthy subjects, not after repeated restriction. Thus the cited paper does not support the claim that repeated restriction was shown to impair both outcomes. (LLM, conf=0.89)
- Supportedcites [14] source
In “Obesity, Diabetes and Sleep Loss: Evidence from Laboratory Studies” (page not provided), the review describes controlled bedtime restriction in young adults and reports decreased insulin sensitivity and glucose tolerance after repeated short nights. It also notes consistent findings in follow-up studies. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [15] source
- Supportedcites [16] source
The Abstract describes a controlled sleep-laboratory comparison in 15 healthy men after two nights of restricted versus regular sleep. Its Conclusions report impaired glucose tolerance that appeared to be primarily caused by reduced insulin sensitivity; the Discussion likewise interprets the breakfast glucose and insulin responses as evidence of reduced insulin sensitivity. (LLM, conf=0.90)
- Not checked — no full text of the sourcecites [17] source
boosteddirect- 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.
- Disputed
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“To our knowledge, this finding identifies for the first time a molecular mechanism that may be involved in the reduction in total body insulin sensitivity consistently observed in multiple laboratory studies of partial sleep deprivation in healthy adults (11–17), as well as in the participants of our study.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
What the sources say
- Disputedcites [11] sourceExperimental — accuracy not yet measured
The citation is attached to the claim that laboratory studies consistently observed reduced insulin sensitivity after partial sleep deprivation. In the paper’s “Impact of Sleep Loss on Insulin Sensitivity and Glucose Tolerance” section (p. 271), insulin sensitivity measured by both HOMA-IR and Matsuda index remained unchanged after sleep loss in healthy women. The paper therefore reports a contrary result, although it notes an association between individual changes in energy expenditure and insulin sensitivity. (LLM, conf=0.86)
Checked by a reasoning model — may be wrong.
- Supportedcites [12] source
The Discussion reports that one week of sleep restriction significantly reduced insulin sensitivity in healthy men, measured by two methods. The citation identifies this paper as one of the laboratory studies behind the sentence; the proposed molecular mechanism is the citing authors’ own finding, not a finding attributed to this source. Page numbers are unavailable in our copy. (LLM, conf=0.90)
- Supportedcites [13] source
The citation supports the reported reduction in insulin sensitivity after partial sleep deprivation in healthy adults. The Discussion reports a 19–25% reduction after one restricted night. The proposed molecular mechanism is the citing authors’ own finding, not a finding attributed to this source. (LLM, conf=0.90)
- Supportedcites [14] source
The citation supports the background finding, not the citing authors’ claim to have identified a molecular mechanism. In “Obesity, Diabetes and Sleep Loss: Evidence from Laboratory Studies,” the source reports decreased insulin sensitivity after partial sleep restriction and says several follow-up studies found consistent results; the studies involved young to middle-aged adults. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites [15] source
- Supportedcites [16] source
The citation supports the reference to laboratory studies of reduced insulin sensitivity after partial sleep deprivation, not the citing authors’ claim that their own finding identifies a molecular mechanism. In the Discussion (page unavailable), Schmid et al. report that two nights of restricted sleep in healthy men produced a response pointing to reduced insulin sensitivity. The paper does not establish the citing authors’ molecular mechanism, but that is not the point attributed to this source. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [17] 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.
- Disputed
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The approximate 30% reduction in cellular insulin signaling in adipocytes induced by 4 nights of sleep restriction lies within the range of the difference in insulin sensitivity in adipocytes from obese versus lean participants (30) and from diabetic patients versus nondiabetic participants (31).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
What the sources say
- Supportedcites [30] source
The Results (p. 1249) report lower insulin-stimulated glucose transport in adipocytes from patients with diabetes than in those from nondiabetic controls. The Results also report an approximately 40% reduction in maximal transport and a 32% reduction in maximal glucose utilization, making the cited comparison with an approximately 30% reduction reasonable. This paper is cited for the diabetic-versus-nondiabetic comparison, not for the sleep-restriction finding. (LLM, conf=0.84)
- Could not verifycites [31] sourceExperimental — accuracy not yet measured
The citation is attached to the obese-versus-lean adipocyte comparison. Our copy studies lean young subjects, and the Postmeal glucose and insulin responses section says HOMA was used to measure meal responses, not insulin sensitivity. Searches for adipocyte insulin sensitivity and obese-versus-lean differences found no passage supporting the comparison; the paper's approximately 30% figure concerns glucose tolerance and insulin response to intravenous glucose, not adipocyte signaling. (LLM, conf=0.74)
plaincorrelational- 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.
- Supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In all but 1 participant, the insulin-dependent response curve was shifted to the right or the maximal pAkt–tAkt ratio was decreased after sleep restriction compared with normal sleep.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Cellular Insulin Sensitivity in Adipocytes
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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The total AUC of the pAkt–tAkt response to insulin was 30% lower after sleep restriction than after normal sleep (mean AUC of the pAkt–tAkt response to insulin, 893.00 [SD, 208.00] vs. 1280.00 [SD, 190.00]; mean difference, −387.00 [SD, 284.00]; P = 0.01).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Cellular Insulin Sensitivity in Adipocytes
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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The insulin concentration for the half-maximal pAkt–tAkt response was nearly 3-fold higher (mean, 0.71 nM [SD, 0.27] vs. 0.24 nM [SD, 0.24]; P = 0.01; mean difference, 0.47 nM [SD, 0.33]; P = 0.01), and the total area under the receiver-operating characteristic curve of the pAkt–tAkt response was 30% lower (P = 0.01) during sleep restriction than during normal sleep.”
- Also stated in: § Cellular Insulin Sensitivity in Adipocytes · plain
“In addition, the insulin concentration corresponding to the half-maximal pAkt–tAkt response was nearly tripled after sleep restriction than after normal sleep (0.71 nM [SD, 0.27] vs. 0.24 nM [SD, 0.24]; mean difference, 0.47 nM [SD, 0.33]; P = 0.01).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Abstract > Results
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.
- Also stated in: § Cellular Insulin Sensitivity in Adipocytes · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Finally, the maximum insulin-induced pAkt–tAkt response was reduced by 29% (106 [SD, 23] vs. 150 [SD, 23]; mean difference, −44 [SD, 36]; P = 0.02) during sleep restriction compared with normal sleep.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Cellular Insulin Sensitivity in Adipocytes
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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Sleep restriction consistently induced a marked reduction in the pAkt response to insulin (Figure 1, right column).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Cellular Insulin Sensitivity in Adipocytes
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.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Total body insulin sensitivity was reduced by 16% after 4 days of sleep restriction compared with normal sleep (3.77 [mU/L]−1 per min−1 [SD, 1.06] vs. 3.22 [mU/L]−1 per min−1 [SD, 1.38]; mean difference, −0.58 [mU/L]−1 per min−1 [SD, 0.51]; P = 0.02).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Total Body Insulin Sensitivity
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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast, tAkt levels did not change across study conditions or insulin concentrations (Appendix Figure).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Cellular Insulin Sensitivity in Adipocytes
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. 14
- Probably not a substantial claim. 10
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Insufficient sleep increases the risk for insulin resistance, type 2 diabetes, and obesity, suggesting that sleep restriction may impair peripheral metabolic pathways.”
- Also stated in: § Primary Funding Source · hedged
“prospective epidemiologic studies have found that insufficient sleep may increase the risk for metabolic disturbances, including insulin resistance, obesity, and type 2 diabetes (4–10).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Abstract > Background
What the sources say
- Not checked — no full text of the sourcecites [4] source
- Partly supportedcites [5] sourceExperimental — accuracy not yet measured
The Results (Short duration of sleep; page not supplied) associate short sleep with a higher incidence of type 2 diabetes. The paper links reduced sleep to insulin resistance through short-term and cross-sectional studies, not prospective evidence; its Conclusions (Potential mechanisms; page not supplied) describe obesity as a possible consequence rather than a demonstrated prospective outcome. The cited evidence therefore does not support attributing all three risks to prospective studies. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [6] source
- Partly supportedcites [7] sourceExperimental — accuracy not yet measured
The Results (page unavailable) report that adults sleeping six hours or less had a higher adjusted risk of developing type 2 diabetes or impaired glucose tolerance. The Introduction and Discussion link short sleep to overweight and cite physiological evidence of insulin resistance, but this prospective study does not establish an increased risk of developing either obesity or insulin resistance. Its Discussion also cautions that a causal role for sleep curtailment remains uncertain. (LLM, conf=0.86)
- Partly supportedcites [8] sourceExperimental — accuracy not yet measured
The “Sleep and diabetes” section reports that prospective studies associate short sleep with incident diabetes, and “Sleep and BMI, obesity and appetite regulation” reports prospective associations with weight gain and childhood obesity. The paper discusses insulin resistance as a possible metabolic consequence in “Potential Mechanisms,” not as a risk established by prospective epidemiologic studies. It also cautions that observational evidence does not establish the causal claim that insufficient sleep increases these risks. Page numbers are unavailable in our copy. (LLM, conf=0.87)
- Partly supportedcites [9] sourceExperimental — accuracy not yet measured
The prospective cohort studies section reports that short sleep duration is associated with increased weight gain and obesity risk. The review does not establish increased risk of insulin resistance or type 2 diabetes; its epidemiology discussion also says a causal link between short sleep and obesity remains to be established. The citing sentence’s causal wording therefore overstates the review. (LLM, conf=0.88)
- Partly supportedcites [10] sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) reports prospective evidence linking short sleep with incident type 2 diabetes and observational evidence linking inadequate sleep with obesity. The Results and Discussion (page unavailable) link short sleep to incident impaired fasting glucose and discuss insulin resistance as a possible mediator, but do not establish a higher risk of developing insulin resistance. The paper does not present prospective evidence for all three outcomes. (LLM, conf=0.88)
plaincorrelational- 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.
- Also stated in: § Primary Funding Source · hedged
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
“This test has been used to show an adverse effect of sleep disturbances on human glucose metabolism and insulin sensitivity in multiple previous reports (12, 15,17, 23, 24). In 1 study that used both the FSIVGTT and the euglycemic hyperinsulinemic clamp to assess changes in insulin sensitivity after experimental sleep restriction in healthy participants, both methods provided similar results (12).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > FSIVGTT
What the sources say
- Supportedcites [12] source
The Results (Insulin sensitivity and acute insulin response) report reduced insulin sensitivity and glucose tolerance after sleep restriction using the IVGTT. The Discussion explicitly says this study used both the insulin-modified FSIVGTT and the euglycemic-hyperinsulinemic clamp, with concordant results. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites [15] source
- Not checked — no full text of the sourcecites [17] source
- Supportedcites [23] source
The Study Protocol says the IVGTT was performed before and after two nights of sleep fragmentation. The Results report decreases in insulin sensitivity and glucose effectiveness, supporting this paper as one of the cited reports using the test to show adverse metabolic effects. The separate comparison with a euglycemic clamp is explicitly attributed to reference 12, not to this paper. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [24] 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.
- Supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Indeed, exogenous administration of cortisol or norepinephrine, 2 hormones that are hypersecreted when the hypothalamic–pituitary–adrenal axis and sympathetic nervous system are respectively activated, has been shown to induce total body (36–38) and cellular (39) insulin resistance.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
What the sources say
- Not checked — no full text of the sourcecites [36] source
- Not checked — no full text of the sourcecites [37] source
- Not checked — no full text of the sourcecites [38] source
- Could not verifycites [39] sourceExperimental — accuracy not yet measured
The Discussion links free-fatty-acid bursts to possible obesity-related insulin resistance, but does not report that administering cortisol or norepinephrine induces insulin resistance. Searches for cortisol, norepinephrine administration, and insulin resistance found no passage establishing the claimed whole-body or cellular effect. (LLM, conf=0.76)
boosteddirect- 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 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
“Both reduced leptin levels (32, 33) and elevated free fatty acid concentrations (13) have been observed in healthy persons after experimental sleep restriction and could conceivably contribute to increased risk for obesity and diabetes.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
What the sources say
- Not checked — no full text of the sourcecites [32] source
- Could not verifycites [33] sourceExperimental — accuracy not yet measured
The Discussion reports associations between self-reported sleep and cortisol secretion in the Whitehall II cohort, not an experimental sleep-restriction study. Searches of our copy for free fatty acids and leptin found no passage reporting the claimed changes in either measure. (LLM, conf=0.78)
- Supportedcites [13] source
Citation (13) is attached to the elevated free-fatty-acid finding, not the reduced-leptin finding, which cites (32, 33). The Results and Table 1 report higher nonesterified fatty acid concentrations in nine healthy subjects after sleep restriction during the hyperinsulinemic clamp (68 versus 57 µmol/L; P = 0.005); basal concentrations did not increase. (LLM, conf=0.91)
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.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Further, our finding of marked alterations in adipocyte function after experimental sleep restriction challenges the widely held belief that the primary function of sleep is the restoration of central nervous system function (26–29) and suggests that sleep may play an equally important role in peripheral energy metabolism.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
What the sources say
- Partly supportedcites [26] sourceExperimental — accuracy not yet measured
The Abstract (page unavailable) says most theories assign NREM sleep a role in nervous-system recuperation, supporting the claim that this is a common view. It also names energy conservation as a role and does not say CNS restoration is believed to be sleep’s primary function. The citation is attached to that belief, not to the citing authors’ finding about adipocytes or their conclusion about peripheral metabolism. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [27] source
- Partly supportedcites [28] sourceExperimental — accuracy not yet measured
The Background (p. 1) presents restoration of brain function as a traditional view of sleep, and the discussion of sleep homeostasis (p. 5) cites evidence that sleep reverses changes in the brain caused by wakefulness. But the paper treats whether sleep has one primary function as an open question (p. 5); it does not endorse CNS restoration as the primary function. The adipocyte finding and inference about peripheral metabolism are the citing authors’ own, not claims attributed to this source. (LLM, conf=0.82)
- Could not verifycites [29] sourceExperimental — accuracy not yet measured
The Abstract and Discussion (page numbers unavailable) address insulin signalling and glucose transport in adipocytes from obese women, not sleep. Searches for sleep restriction and restoration of central nervous system function found no passage addressing the belief to which the citation is attached. (LLM, conf=0.75)
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.
- Partly supported
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Wrist activity was monitored continuously by using Actiwatch (Philips/Respironics, Andover, Massachusetts) to verify adherence to standardized bedtime schedules.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > Experimental Protocol
plain- 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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“No significant changes occurred in body weight (mean body weight, 72.6 kg [SD, 10.5] under the normal sleep condition vs. 72.4 kg [SD, 9.8] under the sleep restriction condition; mean difference, 0.3 kg [SD, 1.5]; P = 0.67) or percentage of body fat (mean percentage of body fat, 22.3% [SD, 5.5%]; vs. 21.8% [SD, 5.0%]; mean difference, 0.5% [SD, 2.9%]; P = 0.66) across the entire protocol.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results
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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Lysates collected from the same participant under both sleep conditions were simultaneously separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis, then transferred to a nitrocellulose membrane. Membranes containing all samples from each participant were blocked in TBST+ (Tris-buffered saline, containing 0.1% Tween [Sigma-Aldrich], and 5% nonfat dried milk) and immunoblotted in the”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > Insulin-Signaling Assay
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.
Probably not a substantial claim. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“This was a single-center study with a small sample size, and our sample included only 1 woman. The findings will therefore need to be replicated in a larger and more diverse population.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
plain- 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. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Random assignments (ordering of the sleep conditions) were made using computer-generated random numbers and concealed with sealed envelopes.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > Experimental Protocol
plain- 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. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“We assessed cellular insulin sensitivity in adipocytes by examining only pAkt. Because of the limited yield of adipose tissue from our lean participants, we could not assess other components of the insulin-signaling cascade.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
plain- 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. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Over the 4 nights, participants slept an average of 7.87 hours (SD, 0.31) under the normal sleep condition versus 4.35 hours (SD, 0.12) under the sleep restriction condition (mean difference, 3.53 hours [SD, 0.24]; P < 0.001).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Polysomnography
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.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Caloric intake was strictly controlled and identical under the 2 sleep conditions.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > Experimental Protocol
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.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Randomized, 2-period, 2-condition, crossover clinical study.”
- Also stated in: § Methods · plain
“Participants were tested under 2 experimental conditions in randomized order—after 4 consecutive nights of 8.5 hours in bed (normal sleep) and 4 consecutive nights of 4.5 hours in bed (sleep restriction).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Abstract > Design
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.
Probably not a substantial claim.
- Also stated in: § Methods · plain
In the paper
“Sleep was recorded by polysomnography (Neurofax EEG-1100A, Nihon Kohden, Foothill Ranch, California) each night. The recordings were visually scored in 30-second epochs as rapid eye movement (REM) sleep, non-REM sleep, and wake according to standard criteria (20).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > Experimental Protocol
What the sources say
- Not checked — no full text of the sourcecites [20] source
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.
Probably not a substantial claim. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The second biopsy was performed at the opposite side of the first biopsy (also within a 9-cm radius of the umbilicus) to obviate the potential effect of local inflammation on insulin sensitivity.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > Biopsy of Subcutaneous Abdominal Fat
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.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Sleep restriction in our study was relatively severe and maintained over a short period of 4 days.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
plain- 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. 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
“Our findings also shed novel light on the still-elusive function of sleep, traditionally conceptualized as necessary only for the brain, because they suggest that sleep plays an important role for the functional integrity of multiple peripheral cell types, as well as for whole-body energy homeostasis.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
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.
The paper relies on this without support.
Before this study, no studies had linked sleep restriction to alterations in molecular metabolic pathways in any peripheral human tissue.
“To our knowledge, no studies to date have linked sleep restriction to alterations in molecular metabolic pathways in any peripheral human tissue.”
The paper relies on this without support.
Phosphorylation of Akt is a crucial step in the insulin-signaling pathway and a valid measure of cellular insulin sensitivity.
“The ability of insulin to increase levels of phosphorylated Akt (pAkt), a crucial step in the insulin-signaling pathway, was assessed.”
“Phosphorylation of Akt, a crucial step of the phosphatidylinositol 3-kinase (PI3K) pathway that mediates most metabolic actions of insulin, was markedly impaired after sleep restriction.”
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 cited source says what the claim attributes to it.
In the citing paper
“Experimental sleep restriction in healthy adults results in increases in insulin resistance99 and decreases in insulin sensitivity.81”
From Sleep Duration and Quality: Impact on Lifestyle Behaviors and Cardiometabolic Health: A Scientific Statement From the American Heart Association (2016) · cites this paper as [99]
In the citing paper
“Therefore, while no changes to Glut4 mRNA or protein content were observed in tandem with changes in glucose tolerance, it is plausible that GLUT4 translocation to the cell membrane may be impaired, which would support previous research that has indicated impairments within the insulin signaling pathway following sleep restriction [52,53].”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [52]
In the citing paper
“Several well-controlled laboratory studies have consistently shown marked reductions in insulin sensitivity in young adults following sleep loss [2–7].”
From Sleep restriction increases free fatty acids in healthy men (2015) · cites this paper as [6]
In the citing paper
“Our current finding of elevated NEFA also suggests that adipocytes are resistant to the antilipolytic effects of insulin”
From Sleep restriction increases free fatty acids in healthy men (2015) · cites this paper as [6]
In the citing paper
“Sleep restriction increased the required insulin concentration to achieve half-maximal pAkt/tAkt response 3-fold, demonstrating impaired insulin signaling in abdominal fat tissue after partial sleep restriction.”
From Metabolic effects of sleep disruption, links to obesity and diabetes (2014) · cites this paper as [33]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Total Body Insulin Sensitivity
“Total body insulin sensitivity was reduced by 16% after 4 days of sleep restriction compared with normal sleep (3.77 [mU/L]−1 per min−1 [SD, 1.06] vs. 3.22 [mU/L]−1 per min−1 [SD, 1.38];”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Total Body Insulin Sensitivity
“mean difference, −0.58 [mU/L]−1 per min−1 [SD, 0.51]; P = 0.02).”
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Cited by
Sorted by citations
Items 101–200 of 360
Wang, Z., Yang, W., Li, X., Qi, X., Pan, K., & Xu, W. (2022) · Journal of the American Heart Association · doi:10.1161/jaha.122.025969 · Cited by 60
Ding, C., Lim, L., Li, X., & Kong, A. P. S. (2018) · Journal of Obesity & Metabolic Syndrome · doi:10.7570/jomes.2018.27.1.4 · Cited by 81
Type 2 diabetes and cardiovascular disease: what next?
Joseph, J. J., & Golden, S. H. (2014) · Current Opinion in Endocrinology, Diabetes & Obesity · doi:10.1097/med.0000000000000044 · Cited by 57
“adipocyte insulin resistance [80], hyperglycemia and incident T2DM [81,82], reduced leptin and elevated ghrelin levels [83], elevated afternoon and evening cortisol [79], weight gain [81,82,84], sympathetic nervous system activation and hypertension [85–88].”
BackgroundBiomarkers of cardiovascular risk in sleep-deprived people
Miller, M. A., & Cappuccio, F. P. (2013) · Journal of Human Hypertension · doi:10.1038/jhh.2013.27 · Cited by 57
Two Nights of Recovery Sleep Reverses the Effects of Short-term Sleep Restriction on Diabetes Risk
Broussard, J. L., Wroblewski, K., Kilkus, J. M., & Tasali, E. (2016) · Diabetes Care · doi:10.2337/dc15-2214 · Cited by 56
Self-citationRegnier, S. M., Kirkley, A. G., Ye, H., El‐Hashani, E., Zhang, X., Neel, B. A., Kamau, W., Thomas, C. C., Williams, A. K., Hayes, E. T., et al. (2014) · Endocrinology · doi:10.1210/en.2014-1668 · Cited by 55
Circadian and Sleep Metabolomics Across Species
Malik, D. M., Paschos, G. K., Sehgal, A., & Weljie, A. M. (2020) · Journal of Molecular Biology · doi:10.1016/j.jmb.2020.04.027 · Cited by 54
“Furthermore, circadian rhythms and sleep both play a role in various disorders with underlying metabolic dysfunction such as metabolic [12, 199] and neurodegenerative disorders [10, 200-202].”
BackgroundSleep and circadian disruption and the gut microbiome-possible links to dysregulated metabolism
Withrow, D., Bowers, S. J., Depner, C. M., González, A., Reynolds, A. C., & Wright, K. P. (2020) · Current Opinion in Endocrine and Metabolic Research · doi:10.1016/j.coemr.2020.11.009 · Cited by 58
Kudlow, P. A., Cha, D. S., Lam, R. W. M., & McIntyre, R. S. (2013) · Sleep Medicine · doi:10.1016/j.sleep.2013.04.017 · Cited by 55
Ray, S., & Reddy, A. B. (2016) · BioEssays · doi:10.1002/bies.201500056 · Cited by 50
Thimgan, M. S., Seugnet, L., TURK, J. W., & Shaw, P. J. (2015) · SLEEP · doi:10.5665/sleep.4680 · Cited by 51
Li, Y., Cai, S., Ling, Y., Mi, S., Fan, C., Zhong, Y., & Shen, Q. (2019) · Sleep Medicine · doi:10.1016/j.sleep.2019.03.026 · Cited by 50
Pandalai, S. P., Schulte, P. A., & Miller, D. B. (2013) · Scandinavian Journal of Work Environment & Health · doi:10.5271/sjweh.3363 · Cited by 52
Ford, E. S., Wheaton, A. G., Chapman, D. P., Li, C., Perry, G. S., & Croft, J. B. (2013) · Journal of Diabetes · doi:10.1111/1753-0407.12101 · Cited by 49
Zhang, X., Zhang, R., Cheng, L., Wang, Y., Ding, X., Fu, J., Dang, J., Moore, J., & Li, R. (2020) · Sleep Medicine · doi:10.1016/j.sleep.2020.05.014 · Cited by 50
Bliwise, D. L., Rosen, R. C., & Baum, N. H. (2014) · Neurourology and Urodynamics · doi:10.1002/nau.22585 · Cited by 47
The Architecture of Risk for Type 2 Diabetes: Understanding Asia in the Context of Global Findings
Abdullah, N., Attia, J., Oldmeadow, C. J., Scott, R. J., & Holliday, E. G. (2014) · International Journal of Endocrinology · doi:10.1155/2014/593982 · Cited by 47
“A recent randomized, crossover study found that sleep deprivation impairs peripheral metabolic pathways, thereby reducing insulin sensitivity [69].”
BackgroundRoy, S., Abudu, A., Salinas, I., Sinha, N., Cline-Fedewa, H. M., Yaw, A. M., Qi, W., Lydic, T. A., Takahashi, D. L., Hennebold, J. D., et al. (2022) · Endocrinology · doi:10.1210/endocr/bqac127 · Cited by 44
Circulating Exosomal miRNAs Signal Circadian Misalignment to Peripheral Metabolic Tissues
Khalyfa, A., Gaddameedhi, S., Crooks, E., Zhang, C., Li, Y., Qiao, Z., Trzépizur, W., Kay, S. A., Andrade, J., Satterfield, B. C., et al. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21176396 · Cited by 46
“Similar to our results, reduction of insulin signaling in human adipose tissue analyzed by pAkt/Akt ratio has been reported for subjects with insufficient sleep [87].”
ResultVolden, P. A., Skor, M. N., Johnson, M. B., Singh, P., Patel, F. N., McClintock, M. K., Brady, M., & Conzen, S. D. (2016) · Cancer Prevention Research · doi:10.1158/1940-6207.capr-15-0107 · Cited by 43
“Cells were then dosed with LPA for 10 minutes and then washed with cold PBS, followed by protein harvesting and Western blot analysis, as described previously (20).”
MethodSelf-citationJácome-Sosa, M., Parks, E. J., Bruno, R. S., Tasali, E., Lewis, G. F., Schneeman, B. O., & Rains, T. M. (2016) · Advances in Nutrition · doi:10.3945/an.115.010397 · Cited by 49
“These findings also suggest a mechanism of adipoctye cell resistance to the antilipolytic effects of insulin which is consistent with impaired intracellular insulin signaling in adipose tissue that occurs after sleep restriction (76, 89).”
BackgroundSelf-citationSaner, N. J., Bishop, D. J., & Bartlett, J. D. (2018) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2017.01.001 · Cited by 41
Vincent, G. E., Jay, S. M., Sargent, C., Kovac, K., Vandelanotte, C., Ridgers, N. D., & Ferguson, S. A. (2017) · Neurobiology of Sleep and Circadian Rhythms · doi:10.1016/j.nbscr.2017.09.001 · Cited by 42
“Numerous well-controlled laboratory studies have observed impaired glucose metabolism with varying degrees of sleep loss (Broussard et al., 2012; Buxton et al., 2010; Nedeltcheva et al., 2009).”
BackgroundDeveloping preliminary blood metabolomics-based biomarkers of insufficient sleep in humans
Depner, C. M., Cogswell, D. T., Bisesi, P. J., Markwald, R. R., Cruickshank-Quinn, C. I., Quinn, K. D., Melanson, E. L., Reisdorph, N. A., & Wright, K. P. (2020) · SLEEP · doi:10.1093/sleep/zsz321 · Cited by 46
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Short-term moderate sleep restriction decreases insulin sensitivity in young healthy adults
Wang, X., Greer, J., Porter, R. R., Kaur, K., & Youngstedt, S. D. (2016) · Sleep Health · doi:10.1016/j.sleh.2015.11.004 · Cited by 42
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“Ex vivo insulin-stimulated subcutaneous adipose biopsies from sleep-restricted subjects have reduced protein kinase B phosphorylation (5), a key step in the insulin-response cascade that is proximal to hormone sensitive lipase suppression (10, 17, 33).”
BackgroundSleep Loss Disrupts Morning-to-Evening Differences in Human White Adipose Tissue Transcriptome
Wilms, B., Leineweber, E., Mölle, M., Chamorro, R., Pommerenke, C., Salinas, G., Sina, C., Lehnert, H., Oster, H., & Schmid, S. M. (2018) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2018-01663 · Cited by 41
“In line with the current study, it has been previously shown that two nights of sleep restriction with only 4 hours of sleep induce an insulin-resistant state in the human adipocyte together with a reduction of total body insulin sensitivity (30).”
BackgroundEndocrine Physiology in Relation to Sleep and Sleep Disturbances
Cauter, E. V., & Tasali, E. (2011) · Elsevier eBooks · doi:10.1016/b978-1-4160-6645-3.00026-8 · Cited by 38
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Type 1 Diabetes, Sleep, and Hypoglycemia
Zhu, B., Irsheed, G. A., Martyn-Nemeth, P. A., & Reutrakul, S. (2021) · Current Diabetes Reports · doi:10.1007/s11892-021-01424-1 · Cited by 38
Pizinger, T., Aggarwal, B., & St‐Onge, M. (2018) · Frontiers in Endocrinology · doi:10.3389/fendo.2018.00392 · Cited by 36
A Model of Adolescent Sleep Health and Risk for Type 2 Diabetes
Simon, S. L., HIGGINS, J. A., Melanson, E. L., Wright, K. P., & Nadeau, K. J. (2021) · Current Diabetes Reports · doi:10.1007/s11892-020-01373-1 · Cited by 44
de Souza, J. F. T., Dáttilo, M., de Mello, M. T., Tufik, S., & Antunes, H. K. M. (2017) · Frontiers in Physiology · doi:10.3389/fphys.2017.00992 · Cited by 35
“Changes in glucose metabolism following a period of sleep deprivation can be explained by decreased phosphorylation of PI3K/Akt that is closely linked to insulin signaling (Broussard et al., 2012).”
BackgroundThe Effect of Sleep Disruption on Cardiometabolic Health
Hong, S., Lee, D.-B., Yoon, D. W., Yoo, S.-L., & Kim, J. (2025) · Life · doi:10.3390/life15010060 · Cited by 51
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“[27] reported that sleep restriction reduced insulin sensitivity in 17 healthy adults in a randomized4-day crossover clinical studyof either 4.”
BackgroundShort Sleep, Insomnia, and Cardiovascular Disease
Hsieh, C. G., & Martin, J. L. (2019) · Current Sleep Medicine Reports · doi:10.1007/s40675-019-00157-8 · Cited by 36
Vanini, G. (2015) · SLEEP · doi:10.5665/sleep.5334 · Cited by 36
Selvamani, Y., Perianayagam, A., Chaudhary, M., & Himanshu, H. (2018) · Journal of Public Health · doi:10.1007/s10389-018-0906-8 · Cited by 37
“Previous literature also argues that poor sleep is associated with physiological changes such as impaired glucose tolerance and insulin resistance (Broussard et al. 2012; Keckeis et al. Table 4 Association between sleep problems and poor self-rated health in India and China, SAGE Wave…”
BackgroundSleep Optimization and Diabetes Control: A Review of the Literature
Arora, T., & Taheri, S. (2015) · Diabetes Therapy · doi:10.1007/s13300-015-0141-z · Cited by 34
Obstructive sleep apnoea, insulin resistance and adipocytokines
Lam, D. C.-L., Lam, K. S. L., & Ip, M. (2014) · Clinical Endocrinology · doi:10.1111/cen.12597 · Cited by 33
Sleep Control, GPCRs, and Glucose Metabolism
Tsuneki, H., Sasaoka, T., & Sakurai, T. (2016) · Trends in Endocrinology and Metabolism · doi:10.1016/j.tem.2016.06.011 · Cited by 35
“Although a previous study reported that insulin signaling was only partially impaired in cultured adipocytes from subcutaneous fat biopsy samples from healthy subjects after four nights of sleep restriction [19], a recent in vivo study demonstrated that subchronic sleep restriction (five nights with 4 h of sleep) caus…”
BackgroundSleep loss is a metabolic disorder
Feeney, S. P., McCarthy, J. M., Petruconis, C. R., & Tudor, J. C. (2025) · Science Signaling · doi:10.1126/scisignal.adp9358 · Cited by 38
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“Broussard et al. (2012) have demonstrated that sleep restriction influences whole-body insulin sensitivity which is coupled with an impairment in insulin signaling in adipocytes.”
BackgroundMethodResultInfluentialSleep disturbances: one of the culprits of obesity-related cardiovascular risk?
Muscogiuri, G., Tuccinardi, D., Nicastro, V., Barrea, L., Colao, A., & Savastano, S. (2020) · International Journal of Obesity Supplements · doi:10.1038/s41367-020-0019-z · Cited by 34
“This in turn determined a reduction in total body insulin sensitivity in humans [61].”
BackgroundVanini, G., & Torterolo, P. (2021) · Advances in experimental medicine and biology · doi:10.1007/978-3-030-61663-2_5 · Cited by 36
Circadian Dysfunction in Adipose Tissue: Chronotherapy in Metabolic Diseases
Civelek, E., Civelek, D. Ö., Akyel, Y. K., Durman, D. K., & Okyar, A. (2023) · Biology · doi:10.3390/biology12081077 · Cited by 35
“After four nights of sleep deprivation compared to regular sleep, cellular insulin sensitivity in adipocytes from subcutaneous fat samples reduced by ~30% in healthy, young, lean men and women [152].”
BackgroundThe Cost of Sleep Lost: Implications for Health, Performance, and the Bottom Line
Grandner, M. A. (2018) · American Journal of Health Promotion · doi:10.1177/0890117118790621a · Cited by 31
Khalyfa, A., Castro‐Grattoni, A. L., & Gozal, D. (2019) · Therapeutic Advances in Respiratory Disease · doi:10.1177/1753466619895229 · Cited by 30
Challenges and Opportunities for Applying Wearable Technology to Sleep
Tobin, S. Y., Williams, P., Baron, K. G., Halliday, T. M., & Depner, C. M. (2021) · Sleep Medicine Clinics · doi:10.1016/j.jsmc.2021.07.002 · Cited by 34
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Association of Chronic Insomnia With Mortality and Adverse Renal Outcomes
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de Oliveira, E. M., Visniauskas, B., Sandri, S., Migliorini, S., Andersen, M. L., Tufik, S. B., Fock, R. A., Chagas, J. R., & Čampa, A. (2014) · Obesity · doi:10.1002/oby.20970 · Cited by 30
“individuals without pre-existing diabetes mellitus (11,15-18).”
Transcriptional Signatures of Sleep Duration Discordance in Monozygotic Twins
Watson, N., Buchwald, D., Delrow, J. J., Altemeier, W. A., Vitiello, M. V., Pack, A. I., Bamshad, M. J., Noonan, C., & Gharib, S. A. (2017) · SLEEP · doi:10.1093/sleep/zsw019 · Cited by 33
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Gut microbiota alterations in response to sleep length among African-origin adults
Fei, N., Choo-Kang, C., Reutrakul, S., Crowley, S. J., Rae, D. E., Bedu-Addo, K., Plange‐Rhule, J., Forrester, T., Lambert, E. V., Bovet, P., et al. (2021) · PLoS ONE · doi:10.1371/journal.pone.0255323 · Cited by 31
“These include increased inflammatory markers [14], increased sympathetic nervous system activity [13], abnormal cortisol rhythmicity [13], alterations in appetite regulating hormones and food intake [16], and adipocyte dysfunction [15] which altogether contribute to insulin resistance, diabetes and obesity risks.”
BackgroundThe role of sleep duration in diabetes and glucose control
Alnaji, A., Law, G. R., & SCOTT, E. M. (2016) · Proceedings of The Nutrition Society · doi:10.1017/s002966511600063x · Cited by 29
“, 2012((26)) USA Seven young healthy participants Crossover clinical study Sleep restriction Insulin sensitivity Positive association”
BackgroundAl‐Zahrani, M. S., Alhassani, A. A., & Zawawi, K. H. (2020) · Sleep And Breathing · doi:10.1007/s11325-020-02131-z · Cited by 29
Kaar, J. L., Luberto, C. M., Campbell, K. A., & Huffman, J. C. (2017) · World Journal of Cardiology · doi:10.4330/wjc.v9.i5.396 · Cited by 28
Sleep characteristics and HbA1c in patients with type 2 diabetes on glucose-lowering medication
Tan, X. W., & Benedict, C. (2020) · BMJ Open Diabetes Research & Care · doi:10.1136/bmjdrc-2020-001702 · Cited by 28
Modafinil Reduces Neuronal Pyroptosis and Cognitive Decline After Sleep Deprivation
Xiong, X., Zuo, Y., Cheng, L., Yin, Z., Hu, T., Guo, M., Han, Z., Ge, X., Li, W., Wang, Y., et al. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.816752 · Cited by 27
“, 2017), induction of metabolic and cardiovascular diseases (Broussard et al., 2012; Huang et al., 2020), and immune dysfunction (Bryant et al.”
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Circadian rhythms and metabolism: from the brain to the gut and back again
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Metadata
- Authors
- Broussard, J. L., Ehrmann, D. A., Van Cauter, E., Tasali, E., & Brady, M. J.
- Affiliations
- University of Chicago (US)
- From the University of Chicago, Chicago, Illinois.
- Venue
- Annals of Internal Medicine
- Publisher
- American College of Physicians
- Published
- 2012-10-16
- Volume
- 157
- Issue
- 8
- Pages
- 549-557
- ISSN
- 0003-4819 (ISSN-L)
- 1539-3704
- PMC
- PMC4435718
- OpenAlex
- W2013808563
- Cited by
- 364
- References
- 46
- Citations by year
- 2026: 16 · 2025: 24 · 2024: 23 · 2023: 23 · 2022: 32 · 2021: 30 · 2020: 27 · 2019: 23 · 2018: 24 · 2017: 27 · 2016: 28 · 2015: 30 · 2014: 28 · 2013: 24 · 2012: 4
- FWCI
- 36.86
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annals of Internal Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Georgia Clinical and Translational Science Alliance
- National Institutes of Health (DK020595, RR024999)
- National Institute on Aging (P01AG011412)
- National Heart, Lung, and Blood Institute (R01HL086459, T32HL007909)
- National Institute of Diabetes and Digestive and Kidney Diseases (P60DK020595)
- National Center for Research Resources (P41RR013642, UL1RR024999)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P50HD057796)
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- sleep restriction, insulin resistance, insulin signaling, adipocytes, subcutaneous adipose tissue, Akt phosphorylation, insulin sensitivity, energy metabolism, type 2 diabetes risk, obesity
- MeSH terms
- Adolescent, Adult, Dose-Response Relationship, Drug, Female, Glucose Tolerance Test, Humans, Insulin, Insulin Resistance, Male, Sleep Deprivation, Signal Transduction, Polysomnography, Adipocytes, Cross-Over Studies, Proto-Oncogene Proteins c-akt, Young Adult
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