Evidence map›Paper›PMID 40713970›Full record

ArticleCell reports. Medicine2025

Imeglimin suppresses glucagon secretion and induces a loss of α cell identity.

Takahiro Tsuno, Jinghe Li, Kuniyuki Nishiyama, Yuka Imamura Kawasawa, Ryota Inoue, Esther Ong Yajima, Akira Nishiyama, Shigeharu G Yabe, Tatsuya Kin, Hitoshi Okochi and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

16 authors.

Takahiro TsunoLaboratory of Diabetes and Metabolic Disorders, Institute for Molecular and Cellular Regulation (IMCR), Gunma University, Maebashi 371-8512, Japan; Department of Endocrinology and Metabolism, Graduate School of Medicine, Yokohama City University, Yokohama 236-0004, Japan.
Jinghe LiLaboratory of Diabetes and Metabolic Disorders, Institute for Molecular and Cellular Regulation (IMCR), Gunma University, Maebashi 371-8512, Japan.
Kuniyuki NishiyamaLaboratory of Diabetes and Metabolic Disorders, Institute for Molecular and Cellular Regulation (IMCR), Gunma University, Maebashi 371-8512, Japan.
Yuka Imamura KawasawaPenn State University College of Medicine, Hershey, PA 17033, USA; Animal Genome Institute, Palmyra, PA 17010, USA.
Ryota InoueLaboratory of Diabetes and Metabolic Disorders, Institute for Molecular and Cellular Regulation (IMCR), Gunma University, Maebashi 371-8512, Japan.
Esther Ong YajimaLaboratory of Diabetes and Metabolic Disorders, Institute for Molecular and Cellular Regulation (IMCR), Gunma University, Maebashi 371-8512, Japan.
Akira NishiyamaDepartment of Immunology, Graduate School of Medicine, Yokohama City University, Yokohama 236-0004, Japan.
Shigeharu G YabeDepartment of Regenerative Medicine, National Center for Global Health and Medicine (NCGM), Tokyo 162-8655, Japan.
Tatsuya KinClinical Islet Laboratory and Clinical Islet Transplant Program, University of Alberta, Edmonton, AB T6G 2G5, Canada.
Hitoshi OkochiDepartment of Regenerative Medicine, National Center for Global Health and Medicine (NCGM), Tokyo 162-8655, Japan.
Tomohiko TamuraDepartment of Immunology, Graduate School of Medicine, Yokohama City University, Yokohama 236-0004, Japan; Advanced Medical Research Center, Yokohama City University, Yokohama 236-0004, Japan.
A M James ShapiroClinical Islet Laboratory and Clinical Islet Transplant Program, University of Alberta, Edmonton, AB T6G 2G5, Canada.
Seiichi OyadomariDivision of Molecular Biology, Institute of Advanced Medical Sciences, Tokushima University, 3-18-15 Kuramoto, Tokushima 770-8503, Japan.
Tadahiro KitamuraMetabolic Signal Research Center, Institute for Molecular and Cellular Regulation (IMCR), Gunma University, Maebashi 371-8512, Japan.
Yasuo TerauchiDepartment of Endocrinology and Metabolism, Graduate School of Medicine, Yokohama City University, Yokohama 236-0004, Japan.
Jun ShirakawaLaboratory of Diabetes and Metabolic Disorders, Institute for Molecular and Cellular Regulation (IMCR), Gunma University, Maebashi 371-8512, Japan; Department of Endocrinology and Metabolism, Graduate School of Medicine, Yokohama City University, Yokohama 236-0004, Japan. Electronic address: jshira@gunma-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dysregulated α cell function contributes to the development of diabetes. In this study, we find that treatment with imeglimin, an antidiabetic drug, prevents glucagon release and induces a loss of α cell identity through direct action on α cells. Mechanistically, imeglimin reduces Gsα expression to inhibit the exchange protein directly activated by cyclic adenosine monophosphate 2 (EPAC2)-mediated secretion of glucagon induced by low glucose, gastric inhibitory polypeptide (GIP), or adrenaline in an insulin-independent manner. Imeglimin also attenuates α cell Ca

Indexed as

GlucagonGlucagon-Secreting CellsAnimalsGlucoseHumansMafB Transcription FactorMaleMiceMice, Inbred C57BLGlucagonGlucoseMafB Transcription FactorC/EBP homologous proteindedifferentiationdiabetesglucagonG protein-coupled receptor signalingGsαhuman isletsimegliminMafBα cells

Identifiers

PMID40713970
PMCPMC12432361

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.