Evidence map›Paper›PMID 29458148›Full record

ReviewFree radical biology & medicine2018

Untimely oxidative stress in β-cells leads to diabetes - Role of circadian clock in β-cell function.

J Lee, K Ma, M Moulik, V Yechoor

Open access · greenAbstract readReview
In one paragraph

Review in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

17 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
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  6. Review
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  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Circadian Clocks, Sleep, and Metabolism.Advances in experimental medicine and biology · 2021
    Article
  14. Review
  15. Article
  16. Review
  17. 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

4 authors at 3 institutions in 1 country.

J LeeDiabetes and Beta Cell Biology Center, Division of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Pittsburgh, 200 Lothrop, BST-1058W, Pittsburgh, PA 15261, United States.
K MaDiabetes and Metabolism Research Institute, City of Hope, Duarte, CA, United States.
M MoulikDivision of Cardiology, Department of Pediatrics, Children's Hospital of Pittsburgh and University of Pittsburgh, Pittsburgh, PA, United States.
V YechoorDiabetes and Beta Cell Biology Center, Division of Endocrinology, Diabetes & Metabolism, Department of Medicine, University of Pittsburgh, 200 Lothrop, BST-1058W, Pittsburgh, PA 15261, United States. Electronic address: yechoorv@pitt.edu.
University of Pittsburgh · USChildren's Hospital of Pittsburgh · USCity of Hope · US

Funding

Circadian Clock Control of Adipose Depot Development and FunctionR01DK112794 · NIDDK · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI MA, KE · 2018 to 2021
$1.7M
Circadian Clock and Beta Cell Stress AdaptationR01DK097160 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI YECHOOR, VIJAY K · 2014 to 2018
$1.7M
NIDDK NIH HHS R01 DK097160NIDDK NIH HHS R01 DK112794
6 · The paper itself

Abstract

Diabetes results from a loss of β-cell function. With the number of people with diabetes reaching epidemic proportions globally, understanding mechanisms that are contributing to this increasing prevalence is critical. One such factor has been circadian disruption, with shift-work, light pollution, jet-lag, increased screen time, all acting as potential contributory factors. Though circadian disruption has been epidemiologically associated with diabetes and other metabolic disorders for many decades, it is only recently that there has been a better understanding of the underlying molecular mechanisms. Experimental circadian disruption, via manipulation of environmental or genetic factors using gene-deletion mouse models, has demonstrated the importance of circadian rhythms in whole body metabolism. Genetic disruption of core clock genes, specifically in the β-cells in mice, have, now demonstrated the importance of the intrinsic β-cell clock in regulating function. Recent work has also shown the interaction of the circadian clock and enhancers in β-cells, indicating a highly integrated regulation of transcription and cellular function by the circadian clock. Disruption of either the whole body or only the β-cell clock leads to significant impairment of mitochondrial function, uncoupling, impaired vesicular transport, oxidative stress in β-cells and finally impaired glucose-stimulated insulin secretion and diabetes. In this review, we explore the role of the circadian clock in mitigating oxidative stress and preserving β-cell function.

Indexed as

AnimalsCircadian ClocksCircadian RhythmDiabetes MellitusHumansInsulin-Secreting CellsOxidative StressBmal1Circadian clockDiabetesInsulinIsletNrf2Oxidative stressβ-cell

Identifiers

PMID29458148
PMCPMC5910243
OpenAlexW2792400190

What OpenQuestion holds

Textmetadata
LicenceTDM
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.