ReviewDiabetes, obesity & metabolism2015
Circadian control of β-cell function and stress responses.
Review in Diabetes, obesity & metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Pooled it
- Retinal light perception and biological rhythms: The role of light in sleep and mood from an ophthalmic perspective (Review).Molecular medicine reports · 2026Review
- Clock genes in pancreatic disease progression: from circadian regulation to dysfunction.Annals of medicine · 2025Review
- Circadian regulation of insulin secretion in transplanted human stem cell-derived pancreatic β-cells.Stem cell reports · 2025Article
- Origins of Ultrasensitivity and Complex Signaling Dynamics of Cellular Hydrogen Peroxide and Peroxiredoxin.Antioxidants (Basel, Switzerland) · 2025Article
- The role of bHLH-PAS transcription factors in endoplasmic reticulum stress.Frontiers in molecular biosciences · 2025Review
- Core circadian transcription factor Bmal1 mediates β cell response and recovery from pro-inflammatory injury.iScience · 2024Article
- Article
- Pitfalls of Mitochondrial Redox Signaling Research.Antioxidants (Basel, Switzerland) · 2023Review
- Type I Diabetes Pathoetiology and Pathophysiology: Roles of the Gut Microbiome, Pancreatic Cellular Interactions, and the 'Bystander' Activation of Memory CD8International journal of molecular sciences · 2023Review
- The role of circadian clock-controlled mitochondrial dynamics in diabetic cardiomyopathy.Frontiers in immunology · 2023Review
- Emerging Insight Into the Role of Circadian Clock Gene BMAL1 in Cellular Senescence.Frontiers in endocrinology · 2022Review
- Light-Dark Patterns Mirroring Shift Work Accelerate Atherosclerosis and Promote Vulnerable Lesion Phenotypes.Journal of the American Heart Association · 2021Article
- Article
- Proinflammatory Cytokine Interleukin 1β Disrupts β-cell Circadian Clock Function and Regulation of Insulin Secretion.Endocrinology · 2021Article
- Untimely oxidative stress in β-cells leads to diabetes - Role of circadian clock in β-cell function.Free radical biology & medicine · 2018Review
- Circadian Etiology of Type 2 Diabetes Mellitus.Physiology (Bethesda, Md.) · 2018Review
- PERK links the clock and protein stress in cancer.Nature cell biology · 2018Article
- Article
- Alpha TC1 and Beta-TC-6 genomic profiling uncovers both shared and distinct transcriptional regulatory features with their primary islet counterparts.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Circadian disruption is the bane of modern existence and its deleterious effects on health; in particular, diabetes and metabolic syndrome have been well recognized in shift workers. Recent human studies strongly implicate a 'dose-dependent' relationship between circadian disruption and diabetes. Genetic and environmental disruption of the circadian clock in rodents leads to diabetes secondary to β-cell failure. Deletion of Bmal1, a non-redundant core clock gene, leads to defects in β-cell stimulus-secretion coupling, decreased glucose-stimulated ATP production, uncoupling of OXPHOS and impaired glucose-stimulated insulin secretion. Both genetic and environmental circadian disruptions are sufficient to induce oxidative stress and this is mediated by a disruption of the direct transcriptional control of the core molecular clock and Bmal1 on Nrf2, the master antioxidant transcription factor in the β-cell. In addition, circadian disruption also leads to a dysregulation of the unfolded protein response and leads to endoplasmic reticulum stress in β-cells. Both the oxidative and endoplasmic reticulum (ER) stress contribute to an impairment of mitochondrial function and β-cell failure. Understanding the basis of the circadian control of these adaptive stress responses offers hope to target them for pharmacological modulation to prevent and mitigate the deleterious metabolic consequences of circadian disruption.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.