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Cited by 247Pancreatic function and diabetesCircadian rhythm and melatoninSleep and Work-Related Fatigue

Disruption of Circadian Rhythms Accelerates Development of Diabetes through Pancreatic Beta-Cell Loss and Dysfunction

Open access
Gale, John E., Cox, Heather I., Qian, Jingyi, Block, Gene D., Colwell, Christopher S., Matveyenko, Aleksey V.·2011·Journal of Biological Rhythms
DOI 10.1177/0748730411416341PMC PMC3359760
Open this paper in CoChat — free accountOpen PDF

Abstract

Type 2 diabetes mellitus (T2DM) is complex metabolic disease that arises as a consequence of interactions between genetic predisposition and environmental triggers. One recently described environmental trigger associated with development of T2DM is disturbance of circadian rhythms due to shift work, sleep loss, or nocturnal lifestyle. However, the underlying mechanisms behind this association are largely unknown. To address this, the authors examined the metabolic and physiological consequences of experimentally controlled circadian rhythm disruption in wild-type (WT) Sprague Dawley and diabetes-prone human islet amyloid polypeptide transgenic (HIP) rats: a validated model of T2DM. WT and HIP rats at 3 months of age were exposed to 10 weeks of either a normal light regimen (LD: 12:12-h light/dark) or experimental disruption in the light-dark cycle produced by either (1) 6-h advance of the light cycle every 3 days or (2) constant light protocol. Subsequently, blood glucose control, beta-cell function, beta-cell mass, turnover, and insulin sensitivity were examined. In WT rats, 10 weeks of experimental disruption of circadian rhythms failed to significantly alter fasting blood glucose levels, glucose-stimulated insulin secretion, beta-cell mass/turnover, or insulin sensitivity. In contrast, experimental disruption of circadian rhythms in diabetes-prone HIP rats led to accelerated development of diabetes. The mechanism subserving early-onset diabetes was due to accelerated loss of beta-cell function and loss of beta-cell mass attributed to increases in beta-cell apoptosis. Disruption of circadian rhythms may increase the risk of T2DM by accelerating the loss of beta-cell function and mass characteristic in T2DM.

AI snapshot

Written from the paper’s full text.

TL;DR

Experimental disruption of circadian rhythms accelerated diabetes development in diabetes-prone HIP rats but not wild-type rats. The effect was driven by beta-cell loss and dysfunction, with no change in insulin sensitivity.

Key findings

  • In WT rats, 10 weeks of circadian disruption (constant light or 6-h light advance every 3 days) did not significantly alter fasting glucose, glucose- or arginine-stimulated insulin secretion, beta-cell mass/turnover, or insulin sensitivity.
  • In diabetes-prone HIP rats, circadian disruption led to accelerated hyperglycemia; at ~5 months, HIP rats had elevated plasma glucose versus WT (118 ± 2 vs. 107 ± 2, p < 0.01), with more pronounced hyperglycemia in the HIP constant-light group (p < 0.05 for LD vs. LL and 6-h ADV).
  • HIP rats exposed to circadian disruption showed further deterioration in glucose-stimulated insulin secretion (~65% vs. LD, p < 0.05) and arginine-stimulated insulin secretion (~50% vs. LD, p < 0.05).
  • Beta-cell fractional area and mass fell by ~40% versus LD (p < 0.05), associated with increased beta-cell apoptosis (p < 0.05 vs. LD) but no change in beta-cell replication; whole-body insulin sensitivity was comparable across light regimens in both WT and HIP rats.

Methods

  • Male Sprague Dawley WT (n = 43) and diabetes-prone human islet amyloid polypeptide transgenic HIP (n = 33) rats, 3 months old, were assigned for 10 weeks to normal 12:12-h light/dark, 6-h advance of the light cycle every 3 days, or 24-h constant light.
  • Circadian disruption was validated by locomotor activity recordings and plasma melatonin rhythms; metabolic studies included hyperglycemic clamp with arginine bolus, hyperinsulinemic-euglycemic clamp, and pancreatic immunohistochemistry/immunofluorescence for beta-cell mass, apoptosis (TUNEL), and replication (Ki-67).
  • Statistical analysis used ANOVA with Fisher post-hoc where appropriate; significance set at p < 0.05.

Limitations

  • The paper states that the in vivo animal model precludes direct assessment of whether impaired insulin secretion is a direct consequence of beta-cell loss, beta-cell dysfunction, or a combination of both.
  • The paper notes that disrupted feeding behavior associated with constant light and 6-h advances might have influenced results and that additional studies are needed to evaluate this.
  • Evident from the text: findings are from male rats only, use a transgenic diabetes-prone model, and involve a 10-week exposure; human relevance is inferential.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1177/0748730411416341

Cites

43 of 43 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 46 cited sources checked · 0 supported · 0 flagged

  • Findingown data

    Accelerated development of hyperglycemia in HIP rats exposed to constant light or 6-h light advances was not associated with a significant increase in body weight versus normal light-dark conditions.

    “Accelerated development of hyperglycemia in HIP rats exposed to LL or 6-h ADV was not associated with a significant increase in body weight versus LD (Fig. 2D).”
    Quote in the paperNot a substantial claim
  • Findingown data

    In wild-type rats, 10 weeks of experimental disruption of circadian rhythms did not significantly alter fasting blood glucose concentrations.

    “In WT rats, 10 weeks of experimental disruption of circadian rhythms did not significantly alter fasting blood glucose concentrations as well as body weight, implying failure to modify regulation of glucose metabolism (Fig. 2A,C).”
    Quote in the paperNot a substantial claim
  • Findingown data

    The decline in beta-cell mass following exposure of HIP rats to LL and 6-h ADV light regimens was associated with an increased rate of beta-cell apoptosis (p < 0.05 vs LD).

    “This decline in beta-cell mass following exposure to LL and 6-h ADV light regimens was associated with an increased rate of beta-cell apoptosis (p < 0.05 vs. LD; Fig. 4J–L and Fig. 5H) but no change in beta-cell replication (Fig. 4P-R and Fig. 5G).”
    Quote in the paperSubstantial claim
  • Findingown data

    In HIP rats, disruption of circadian rhythms by LL and 6-h ADV led to a significant further deterioration in glucose-stimulated insulin secretion (~65% compared to LD; p < 0.05).

    “HIP rats, disruption of circadian rhythms (LL and 6-h ADV) led to a significant further deterioration in glucose-stimulated (~65% compared to LD; p < 0.05) and arginine-stimulated (~50% compared to LD; p < 0.05) insulin secretion (Fig. 3D–H).”
    Quote in the paperSubstantial claim
  • Findingown data

    In diabetes-prone HIP rats, disruption of circadian rhythms by constant light or 6-h light advances leads to a significant further deterioration in glucose-stimulated insulin secretion, approximately 65% compared with normal light-dark conditions.

    “However, in contrast to WT rats, in diabetes-prone HIP rats, disruption of circadian rhythms (LL and 6-h ADV) led to a significant further deterioration in glucose-stimulated (~65% compared to LD; p <”
    Quote in the paperSubstantial claim
  • May combine two claims. 10
  • Classified as probably not a substantial claim. 16

  • May combine two claims.

    Findingown data

    In WT rats, beta-cell fractional area and beta-cell mass were not altered in LL and 6-h ADV groups compared to LD.

    “in WT rats, beta-cell fractional area, beta-cell mass, and beta-cell turnover (replication and apoptosis) were not altered in LL and 6-h ADV groups compared to LD (Fig. 4A–O and Fig. 5A–F).”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    Body weight in the HIP constant-light group tended to be elevated by approximately 5% from 2 to 10 weeks compared with normal light-dark conditions (p = 0.08).

    “However, body weight in the HIP LL group tended to be elevated ~5% from 2 to 10 weeks (p = 0.08 for LL vs. LD).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    HIP rats develop diabetes by approximately 10 months of age, characterized by progressive loss of pancreatic beta-cell mass and function due to accumulation of toxic human islet amyloid polypeptide oligomers and consequent induction of beta-cell endoplasmic reticulum stress.

    “HIP rats develop diabetes by ~10 months of age, characterized by a progressive loss of pancreatic beta-cell mass and function due to accumulation of toxic human islet amyloid polypeptide oligomers and consequent induction of beta-cell endoplasmic reticulum (ER) stress (Haataja et al., 2008).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Haataja et al., 2008

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    At 3 months of age, HIP rats exhibit fasting glucose levels and beta-cell mass comparable to wild-type rats.

    “At this stage, HIP rats exhibit fasting glucose levels and beta-cell mass comparable to WT rats (Butler et al., 2004).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Butler et al., 2004

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Insulin resistance in type 2 diabetes mellitus primarily manifests at the level of the liver and skeletal muscle, resulting in impaired insulin-stimulated glucose disposal and failure to adequately suppress hepatic glucose production, which contributes to hyperglycemia.

    “Insulin resistance in T2DM primarily manifests at the level of the liver and the skeletal muscle, resulting in impaired insulin-stimulated glucose disposal and failure to adequately suppress hepatic glucose production (DeFronzo et al., 1982), which contributes to hyperglycemia.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites DeFronzo et al., 1982

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    In those vulnerable to T2DM, hyperglycemia occurs as a consequence of impaired insulin secretion in response to insulin resistance.

    “In those vulnerable to T2DM, hyperglycemia occurs as a consequence of impaired insulin secretion in response to insulin resistance (Bergman et al., 1981)”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Bergman et al., 1981

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Most but not all genetic predispositions to type 2 diabetes mellitus appear to be linked to pancreatic beta-cell failure through the regulation of beta-cell function and/or mass.

    “Interestingly, most but not all genetic predispositions to T2DM appear to be linked to pancreatic beta-cell failure through the regulation of beta-cell function and/ or mass (Florez, 2008), whereas most environmental triggers such as obesity and physical inactivity have been shown to primarily influence insulin action (Yki-Jarvinen, 1995).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Florez, 2008

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Misalignment of internal circadian oscillators with the external environment leads to deleterious health consequences and is associated with increased morbidity and mortality in humans.

    “Misalignment of internal circadian oscillators with the external environment leads to deleterious health consequences and has long been associated with increased morbidity and mortality in humans (Reddy and O’Neill, 2010).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Reddy and O’Neill, 2010

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Most environmental triggers such as obesity and physical inactivity primarily influence insulin action.

    “Interestingly, most but not all genetic predispositions to T2DM appear to be linked to pancreatic beta-cell failure through the regulation of beta-cell function and/ or mass (Florez, 2008), whereas most environmental triggers such as obesity and physical inactivity have been shown to primarily influence insulin action (Yki-Jarvinen, 1995).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Yki-Jarvinen, 1995

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductreasoning

    The current study's design precludes direct assessment of whether impaired insulin secretion is a direct consequence of beta-cell loss, beta-cell dysfunction, or a combination of both factors.

    “with the limitation of precluding direct assessment whether resultant impaired insulin secretion is a direct consequence of beta-cell loss, beta-cell dysfunction, or a combination of both factors.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Changes in feeding behavior have the potential to uncouple circadian oscillators in peripheral tissues such as the liver and the pancreas from the SCN, via regulation of peripheral clock gene expression.

    “Changes in feeding behavior have the potential to uncouple circadian oscillators in the peripheral tissues such as the liver and the pancreas from the SCN, via regulation of peripheral clock gene expression (Damiola et al., 2000).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Damiola et al., 2000

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Acute (10 days) circadian misalignment, designed to recapitulate shift work, led to impaired glucose tolerance, fasting hyperglycemia, and diminished beta-cell function.

    “a more recent study demonstrated that acute (10 days) circadian misalignment, designed to recapitulate shift work, led to impaired glucose tolerance, fasting hyperglycemia, and diminished beta-cell function (Scheer et al., 2009).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Scheer et al., 2009

      Not checked in the free run.

  • Classified as probably not a substantial claim. May combine two claims.

    Premisecitation

    Sleep deprivation caused impaired glucose tolerance with decreased beta-cell glucose responsiveness.

    “Spiegel and colleagues (1999) reported that sleep deprivation caused impaired glucose tolerance with decreased beta-cell glucose responsiveness”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Spiegel and colleagues (1999)

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    More than 20% of global gene expression in some peripheral tissues (e.g., liver) is under circadian control.

    “Since more than 20% of global gene expression in some peripheral tissues (e.g., liver) is reported to be under circadian control (Reddy et al., 2006)”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Reddy et al., 2006

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Exposure to LL disrupts locomotor activity and feeding patterns.

    “Both locomotor activity and feeding patterns are disrupted following exposure to LL (Granados-Fuentes et al., 2004), an observation partially confirmed by our studies (Fig. 1).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites Granados-Fuentes et al., 2004

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductreasoning

    Potential aberration of feeding behavior associated with LL and 6-h ADV might have influenced the study's results on pancreatic beta-cell function and survival.

    “Therefore, potential aberration of feeding behavior associated with LL and 6-h ADV might have influenced our results as it pertains to effects on pancreatic beta-cell function and survival.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    The mechanism of beta-cell failure in T2DM shares many parallels with neurodegenerative diseases such as Alzheimer disease.

    “the mechanism of beta-cell failure in T2DM shares many parallels with neurodegenerative diseases such as Alzheimer disease (Haataja et al., 2008).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Haataja et al., 2008

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Sleep loss in humans is associated with an increase in food intake and preference for high-energy foods, which likely contributes to increased risk for obesity, insulin resistance, and subsequently T2DM.

    “sleep loss in humans is associated with an increase in food intake and preference for high-energy foods, which likely contributes to increased risk for obesity, insulin resistance, and, subsequently, T2DM (Spiegel et al., 2005; Van Cauter et al., 2008).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites Spiegel et al., 2005

      Not checked in the free run.

    • cites Van Cauter et al., 2008

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    A role for melatonin in the regulation of glucose homeostasis and beta-cell function was first proposed more than 50 years ago.

    “a role for melatonin in the regulation of glucose homeostasis and beta-cell function was first proposed more than 50 years ago (Milcou et al., 1957).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Milcou et al., 1957

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S2 (checkable), S3 (load-bearing).

    Interpretationreasoning

    Conditions of circadian misalignment that have become commonplace in our "24/7" society may have severe health consequences.

    “emphasize that conditions of circadian misalignment that have become commonplace in our “24/7” society may have severe health consequences.”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: Circadian disruption induced by LL and 6-h ADV in rats models circadian misalignment in humans, such as that caused by shift work.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Melatonin promotes cell survival, particularly in response to Alzheimer beta-amyloid-induced cell death.

    “melatonin has been shown to promote cell survival, particularly in response to Alzheimer beta-amyloid-induced cell death (Jang et al., 2005).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites Jang et al., 2005

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    Melatonin may play a role in the regulation of beta-cell mass and/or function, and disruption of beta-cell melatonin signaling may contribute to development of T2DM associated with circadian rhythm disorders.

    “Collectively, these data imply a possible role for melatonin in the regulation of beta-cell mass and/or function and raise the possibility that disruption of beta-cell melatonin signaling may contribute to development of T2DM associated with circadian rhythm disorders.”
    Quote in the paperSubstantial claim
22 of 22

  • The paper relies on this without support.

    The effects of experimental circadian rhythm disruption in rats are informative about the risk of type 2 diabetes mellitus in humans.

    “Disruption of circadian rhythms may increase the risk of T2DM by accelerating the loss of beta-cell function and mass characteristic in T2DM.”
    “To address this, the authors examined the metabolic and physiological consequences of experimentally controlled circadian rhythm disruption in wild-type (WT) Sprague Dawley and diabetes-prone human islet amyloid polypeptide transgenic (HIP) rats: a validated model of T2DM.”

  • The paper relies on this without support.

    The HIP rat is a valid model of human T2DM in which beta-cell failure is the primary metabolic defect.

    “the primary metabolic defect in HIP rats relates to beta-cell failure”

  • The paper relies on this without support.

    Circadian disruption induced by LL and 6-h ADV in rats models circadian misalignment in humans, such as that caused by shift work.

    “conditions of circadian misalignment that have become commonplace in our “24/7” society may have severe health consequences.”

  • The paper relies on this without support.

    The observed effects on pancreatic beta-cell function and survival are due to circadian disruption rather than other effects of the light schedules.

    “potential aberration of feeding behavior associated with LL and 6-h ADV might have influenced our results as it pertains to effects on pancreatic beta-cell function and survival.”
4 of 4

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?

  • Shift workers or people who sleep poorly are more likely to develop obesity and T2DM due to circadian clock disruption.

    “Shift workers or people who sleep poorly are more likely to develop obesity and T2DM due to circadian clock disruption 31, 32, 33, 34, 35, 36, 37.”

    From The Circadian Syndrome: is the Metabolic Syndrome and much more! (2019) · cites this paper as [33]

  • Circadian disruption may accelerate the development of type 2 diabetes mellitus in diabetes-prone individuals.

    “it is already known that circadian disruption may accelerate the development of T2DM in diabetes-prone individuals.40”

    From Shift work and diabetes mellitus: a meta-analysis of observational studies (2015) · cites this paper as [40]

  • In rats prone to type 2 diabetes, phase advancing the light/dark cycle by 6 h every 3 days for 10 weeks accelerates the onset of type 2 diabetes by causing a hastened loss of beta-cell function and mass.

    “It has also been demonstrated, in rats prone to the development of type 2 diabetes, that phase advancing the light/dark cycle by 6 h every 3 days for 10 weeks accelerates the onset of type 2 diabetes by causing a hastened loss of beta-cell function and mass (Gale et al., 2011).”

    From The impact of the circadian timing system on cardiovascular and metabolic function (2012) · cites this paper as Gale et al., 2011

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.

  • Light-cycle schedule does not return to baseline every 15 days

    Minor

    A 6-hour advance every 3 days requires four advances, or 12 days, to complete a 24-hour cycle and return to the original light schedule. After 15 days, five advances would total 30 hours, leaving the schedule 6 hours from baseline.

  • Bouatia-Naji citation year conflicts with reference list

    Minor

    The in-text citation gives 2000, but the corresponding reference entry gives 2009.

2 of 2

Cites

Flagged first, then by citations

Research works printed but not linked: 2

  1. Kloppel G, 1985, Surv Synth Pathol Res, 4, 110
  2. Milcou SM, 1957, Ann Endocrinol (Paris), 18, 621

Cited by

Sorted by citations

Related

Authors
Gale, J. E., Cox, H. I., Qian, J., Block, G. D., Colwell, C. S., & Matveyenko, A. V.
Affiliations
University of California, Los Angeles (US)
Corresponding author
Matveyenko, Aleksey V.
ORCID
Venue
Journal of Biological Rhythms
Publisher
SAGE Publications
Published
2011-09-15
Volume
26
Issue
5
Pages
423-433
ISSN
  • 0748-7304 (ISSN-L)
  • 1552-4531
DOI
10.1177/0748730411416341
PMC
PMC3359760
OpenAlex
W2021990756
Semantic Scholar
156f0efdddd9aef7987102b1ef9b99213486d7ac
Cited by
247
References
43
Citations by year
2026: 8 · 2025: 13 · 2024: 15 · 2023: 14 · 2022: 8 · 2021: 19 · 2020: 27 · 2019: 18 · 2018: 20 · 2017: 23 · 2016: 13 · 2015: 27 · 2014: 16 · 2013: 14 · 2012: 10
FWCI
13.74
Type
journal article
Language
en
Open access
Licence
journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations
  • Journal of Biological Rhythms (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Larry L. Hillblom Foundation
  • National Institutes of Health
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK063491, K01DK089003, P30DK063491, DK089003)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
Keywords
circadian rhythm disruption, type 2 diabetes, pancreatic beta-cell loss, beta-cell dysfunction, beta-cell apoptosis, beta-cell mass, insulin sensitivity, constant light, glucose-stimulated insulin secretion
MeSH terms
Insulin Secretion, Animals, Blood Glucose, Circadian Rhythm, Diabetes Mellitus, Type 2, Humans, Insulin, Insulin Resistance, Male, Motor Activity, Rats, Sprague-Dawley, Photoperiod, Insulin-Secreting Cells, Rats, Rats, Transgenic, Islet Amyloid Polypeptide

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