Evidence map›Paper›PMID 28886131›Full record

ArticlePloS one2017

Histone deacetylase regulates insulin signaling via two pathways in pancreatic β cells.

Yukina Kawada, Shun-Ichiro Asahara, Yumiko Sugiura, Ayaka Sato, Ayuko Furubayashi, Mao Kawamura, Alberto Bartolome, Emi Terashi-Suzuki, Tomoko Takai, Ayumi Kanno and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
8.4field-weighted citation impact, top 2% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
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  6. Tryptophanylation of insulin receptor by WARS attenuates insulin signaling.Cellular and molecular life sciences : CMLS · 2024
    Article
  7. Epigenetic Regulation of Pancreas Development and Function.Advances in anatomy, embryology, and cell biology · 2024
    Review
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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

14 authors at 2 institutions in 2 countries.

Yukina KawadaDivision of Metabolism and Disease, Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Shun-Ichiro AsaharaDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Yumiko SugiuraDivision of Metabolism and Disease, Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Ayaka SatoMedical Technology Major, Faculty of Health Sciences Major, Kobe University Graduate School of Medicine, Kobe, Japan.
Ayuko FurubayashiMedical Technology Major, Faculty of Health Sciences Major, Kobe University Graduate School of Medicine, Kobe, Japan.
Mao KawamuraMedical Technology Major, Faculty of Health Sciences Major, Kobe University Graduate School of Medicine, Kobe, Japan.
Alberto BartolomeDepartment of Medicine, Columbia University Medical Center, New York, New York, United States of America.
Emi Terashi-SuzukiDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Tomoko TakaiDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Ayumi KannoDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Maki Koyanagi-KimuraDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Tomokazu MatsudaDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Naoko HashimotoDivision of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
Yoshiaki KidoDivision of Metabolism and Disease, Department of Biophysics, Kobe University Graduate School of Health Sciences, Kobe, Japan.
Kobe University · JPColumbia University Irving Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies demonstrated that insulin signaling plays important roles in the regulation of pancreatic β cell mass, the reduction of which is known to be involved in the development of diabetes. However, the mechanism underlying the alteration of insulin signaling in pancreatic β cells remains unclear. The involvement of epigenetic control in the onset of diabetes has also been reported. Thus, we analyzed the epigenetic control of insulin receptor substrate 2 (IRS2) expression in the MIN6 mouse insulinoma cell line. We found concomitant IRS2 up-regulation and enhanced insulin signaling in MIN6 cells, which resulted in an increase in cell proliferation. The H3K9 acetylation status of the Irs2 promoter was positively associated with IRS2 expression. Treatment of MIN6 cells with histone deacetylase inhibitors led to increased IRS2 expression, but this occurred in concert with low insulin signaling. We observed increased IRS2 lysine acetylation as a consequence of histone deacetylase inhibition, a modification that was coupled with a decrease in IRS2 tyrosine phosphorylation. These results suggest that insulin signaling in pancreatic β cells is regulated by histone deacetylases through two novel pathways affecting IRS2: the epigenetic control of IRS2 expression by H3K9 promoter acetylation, and the regulation of IRS2 activity through protein modification. The identification of the histone deacetylase isoform(s) involved in these mechanisms would be a valuable approach for the treatment of type 2 diabetes.

Indexed as

Signal TransductionAcetylationAnimalsCell Line, TumorCell ProliferationDiabetes Mellitus, Type 2Disease Models, AnimalGene ExpressionGene Expression RegulationHistone Deacetylase InhibitorsHistone DeacetylasesHistonesInsulinInsulin Receptor Substrate ProteinsInsulin-Secreting CellsMiceHistone Deacetylase InhibitorsHistone DeacetylasesHistonesInsulinInsulin Receptor Substrate Proteins

Identifiers

PMID28886131
PMCPMC5590960
OpenAlexW2753315619

What OpenQuestion holds

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LicenceCC BY
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.