Evidence map›Paper›PMID 26348474›Full record

ArticleEndocrinology2015

Circadian Disruption and Diet-Induced Obesity Synergize to Promote Development of β-Cell Failure and Diabetes in Male Rats.

Jingyi Qian, Bonnie Yeh, Kuntol Rakshit, Christopher S Colwell, Aleksey V Matveyenko

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.1field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Artificial Light at Night and Type 2 Diabetes Mellitus.Diabetes & metabolism journal · 2024
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Circadian rhythm disruption with high-fat diet impairs glycemic control and bone quality.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Jingyi QianDepartment of Physiology and Biomedical Engineering (K.R., A.V.M.), Mayo Clinic School of Medicine, Mayo Clinic, Rochester, Minnesota 55905; and Department of Medicine (B.Y., A.V.M.) and Laboratory for Circadian and Sleep Medicine (J.Q., C.S.C.), Departments of Psychiatry and Biobehavioral Sciences, University of California Los Angeles, Los Angeles, California 90095.
Bonnie YehDepartment of Physiology and Biomedical Engineering (K.R., A.V.M.), Mayo Clinic School of Medicine, Mayo Clinic, Rochester, Minnesota 55905; and Department of Medicine (B.Y., A.V.M.) and Laboratory for Circadian and Sleep Medicine (J.Q., C.S.C.), Departments of Psychiatry and Biobehavioral Sciences, University of California Los Angeles, Los Angeles, California 90095.
Kuntol RakshitDepartment of Physiology and Biomedical Engineering (K.R., A.V.M.), Mayo Clinic School of Medicine, Mayo Clinic, Rochester, Minnesota 55905; and Department of Medicine (B.Y., A.V.M.) and Laboratory for Circadian and Sleep Medicine (J.Q., C.S.C.), Departments of Psychiatry and Biobehavioral Sciences, University of California Los Angeles, Los Angeles, California 90095.
Christopher S ColwellDepartment of Physiology and Biomedical Engineering (K.R., A.V.M.), Mayo Clinic School of Medicine, Mayo Clinic, Rochester, Minnesota 55905; and Department of Medicine (B.Y., A.V.M.) and Laboratory for Circadian and Sleep Medicine (J.Q., C.S.C.), Departments of Psychiatry and Biobehavioral Sciences, University of California Los Angeles, Los Angeles, California 90095.
Aleksey V MatveyenkoDepartment of Physiology and Biomedical Engineering (K.R., A.V.M.), Mayo Clinic School of Medicine, Mayo Clinic, Rochester, Minnesota 55905; and Department of Medicine (B.Y., A.V.M.) and Laboratory for Circadian and Sleep Medicine (J.Q., C.S.C.), Departments of Psychiatry and Biobehavioral Sciences, University of California Los Angeles, Los Angeles, California 90095.
University of California, Los Angeles · USMayo Clinic in Arizona · US

Funding

Role of Circadian Misalignment in Beta-cell Failure in Type 2 DiabetesR01DK098468 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ALEKSEY V MATVEYENKO · 2013 to 2026
$5.8M
NIDDK NIH HHS DK098468NIDDK NIH HHS R01 DK098468
6 · The paper itself

Abstract

There are clear epidemiological associations between circadian disruption, obesity, and pathogenesis of type 2 diabetes. The mechanisms driving these associations are unclear. In the current study, we hypothesized that continuous exposure to constant light (LL) compromises pancreatic β-cell functional and morphological adaption to diet-induced obesity leading to development of type 2 diabetes. To address this hypothesis, we studied wild type Sprague Dawley as well as Period-1 luciferase reporter transgenic rats (Per1-Luc) for 10 weeks under standard light-dark cycle (LD) or LL with concomitant ad libitum access to either standard chow or 60% high-fat diet (HFD). Exposure to HFD led to a comparable increase in food intake, body weight, and adiposity in both LD- and LL-treated rats. However, LL rats displayed profound loss of behavioral circadian rhythms as well as disrupted pancreatic islet clock function characterized by the impairment in the amplitude and the phase islet clock oscillations. Under LD cycle, HFD did not adversely alter diurnal glycemia, diurnal insulinemia, β-cell secretory function as well as β-cell survival, indicating successful adaptation to increased metabolic demand. In contrast, concomitant exposure to LL and HFD resulted in development of hyperglycemia characterized by loss of diurnal changes in insulin secretion, compromised β-cell function, and induction of β-cell apoptosis. This study suggests that circadian disruption and diet-induced obesity synergize to promote development of β-cell failure, likely mediated as a consequence of impaired islet clock function.

Indexed as

ApoptosisDiet, High-FatPhotoperiodAdiposityAnimalsBiological ClocksBody WeightChronobiology DisordersDiabetes Mellitus, Type 2Disease Models, AnimalGenes, ReporterHyperglycemiaInsulinInsulin-Secreting CellsInsulin SecretionLuciferasesInsulinLuciferasesPer1 protein, ratPeriod Circadian Proteins

Identifiers

PMID26348474
PMCPMC4655211
OpenAlexW1659693438

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.