Evidence map›Paper›PMID 25695910›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2015

Activation of Melatonin Signaling Promotes β-Cell Survival and Function.

Safia Costes, Marti Boss, Anthony P Thomas, Aleksey V Matveyenko

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
9.4field-weighted citation impact, top 1% 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

43 citing papers in PubMed, 79 citations in OpenAlex.

  1. Trial
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  3. Nocturnal melatonin secretion and risk of type 2 diabetes: a prospective cohort study.The Journal of clinical endocrinology and metabolism · 2026
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  9. Diabetes-associated Genetic Variation inJournal of the Endocrine Society · 2024
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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 1 institution in 1 country.

Safia CostesDepartment of Medicine (S.C., M.B., A.P.T., A.V.M.), David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095; and Department of Physiology and Biomedical Engineering (A.V.M.), Mayo Clinic School of Medicine, Mayo Clinic Rochester, Minnesota 55905.
Marti Boss
Anthony P Thomas
Aleksey V Matveyenko
University of California, Los Angeles · 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 R01 DK098468NIDDK NIH HHS R01DK098468
6 · The paper itself

Abstract

Type 2 diabetes mellitus (T2DM) is characterized by pancreatic islet failure due to loss of β-cell secretory function and mass. Studies have identified a link between a variance in the gene encoding melatonin (MT) receptor 2, T2DM, and impaired insulin secretion. This genetic linkage raises the question whether MT signaling plays a role in regulation of β-cell function and survival in T2DM. To address this postulate, we used INS 832/13 cells to test whether activation of MT signaling attenuates proteotoxicity-induced β-cell apoptosis and through which molecular mechanism. We also used nondiabetic and T2DM human islets to test the potential of MT signaling to attenuate deleterious effects of glucotoxicity and T2DM on β-cell function. MT signaling in β-cells (with duration designed to mimic typical nightly exposure) significantly enhanced activation of the cAMP-dependent signal transduction pathway and attenuated proteotoxicity-induced β-cell apoptosis evidenced by reduced caspase-3 cleavage (∼40%), decreased activation of stress-activated protein kinase/Jun-amino-terminal kinase (∼50%) and diminished oxidative stress response. Activation of MT signaling in human islets was shown to restore glucose-stimulated insulin secretion in islets exposed to chronic hyperglycemia as well as in T2DM islets. Our data suggest that β-cell MT signaling is important for the regulation of β-cell survival and function and implies a preventative and therapeutic potential for preservation of β-cell mass and function in T2DM.

Indexed as

AnimalsCell Line, TumorCell SurvivalDiabetes Mellitus, Type 2HumansInsulin-Secreting CellsMelatoninRatsReceptors, MelatoninSignal TransductionMelatoninReceptors, Melatonin

Identifiers

PMID25695910
PMCPMC4415205
OpenAlexW2145215846

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.