Evidence map›Paper›PMID 32455427›Full record

ArticleEndocrinology2021

Proinflammatory Cytokine Interleukin 1β Disrupts β-cell Circadian Clock Function and Regulation of Insulin Secretion.

Naureen Javeed, Matthew R Brown, Kuntol Rakshit, Tracy Her, Satish K Sen, Aleksey V Matveyenko

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Naureen JaveedDepartment of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Matthew R BrownDepartment of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Kuntol RakshitDepartment of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Tracy HerDepartment of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Satish K SenDepartment of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Aleksey V MatveyenkoDepartment of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine and Science, Rochester, Minnesota.
Mayo Clinic · 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
Interdisciplinary Training in Lung Physiology and Biomedical EngineeringT32HL105355 · NHLBI · MAYO CLINIC ROCHESTER · PI PRAKASH, Y. S., SIECK, GARY C. · 2012 to 2021
$3.9M
NBCe1-mediated Regulation of HCO3- is a Novel Mechanism Underlying Metabolic Reprogramming and CystogenesisF99DK123834 · NIDDK · MAYO CLINIC ROCHESTER · PI BROWN, MATTHEW · 2019 to 2020
$92k
NHLBI NIH HHS T32 HL105355NIDDK NIH HHS F99 DK123834NIDDK NIH HHS R01 DK098468
6 · The paper itself

Abstract

Intrinsic β-cell circadian clocks are important regulators of insulin secretion and overall glucose homeostasis. Whether the circadian clock in β-cells is perturbed following exposure to prodiabetogenic stressors such as proinflammatory cytokines, and whether these perturbations are featured during the development of diabetes, remains unknown. To address this, we examined the effects of cytokine-mediated inflammation common to the pathophysiology of diabetes, on the physiological and molecular regulation of the β-cell circadian clock. Specifically, we provide evidence that the key diabetogenic cytokine IL-1β disrupts functionality of the β-cell circadian clock and impairs circadian regulation of glucose-stimulated insulin secretion. The deleterious effects of IL-1β on the circadian clock were attributed to impaired expression of key circadian transcription factor Bmal1, and its regulator, the NAD-dependent deacetylase, Sirtuin 1 (SIRT1). Moreover, we also identified that Type 2 diabetes in humans is associated with reduced immunoreactivity of β-cell BMAL1 and SIRT1, suggestive of a potential causative link between islet inflammation, circadian clock disruption, and β-cell failure. These data suggest that the circadian clock in β-cells is perturbed following exposure to proinflammatory stressors and highlights the potential for therapeutic targeting of the circadian system for treatment for β-cell failure in diabetes.

Indexed as

AgedAnimalsARNTL Transcription FactorsCircadian ClocksDiabetes Mellitus, Type 2FemaleGene Expression RegulationHumansInsulinInsulinomaInsulin-Secreting CellsInterleukin-1betaMaleMiceMice, KnockoutMice, TransgenicARNTL Transcription FactorsBMAL1 protein, humanBmal1 protein, mouseInsulinInterleukin-1betaNuclear Receptor Subfamily 1, Group F, Member 1RORA protein, humanSirtuinscircadian clockcytokinesdiabetesinflammationβ-cell

Identifiers

PMID32455427
PMCPMC7692023
OpenAlexW3030780584

What OpenQuestion holds

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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.