Evidence map›Paper›PMID 34523242›Full record

ArticleJournal of diabetes investigation2022

A novel mechanism of imeglimin-mediated insulin secretion via the cADPR-TRP channel pathway.

Shunsuke Funazaki, Masashi Yoshida, Hodaka Yamada, Masafumi Kakei, Masanobu Kawakami, Shuichi Nagashima, Kazuo Hara, Katsuya Dezaki

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
5.0field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  16. Improving the Effects of Imeglimin on Endothelial Function: A Prospective, Single-Center, Observational Study.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2023
    Article
  17. Article
  18. Review
  19. 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

8 authors at 1 institution in 1 country.

Shunsuke FunazakiDepartment of Medicine, Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan.ORCID https://orcid.org/0000-0002-3323-1310
Masashi YoshidaDepartment of Medicine, Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan.
Hodaka YamadaDepartment of Medicine, Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan.ORCID https://orcid.org/0000-0002-1882-1814
Masafumi KakeiDepartment of Medicine, Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan.
Masanobu KawakamiDepartment of Medicine, Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan.
Shuichi NagashimaDepartment of Medicine, Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan.ORCID https://orcid.org/0000-0003-2509-8588
Kazuo HaraDepartment of Medicine, Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan.
Katsuya DezakiDepartment of Physiology, Division of Integrative Physiology, Jichi Medical University, Shimotsuke-shi, Japan.
Jichi Medical University · JP

Funding

Japan Society for the Promotion of Science 18K08524Japan Society for the Promotion of Science 18K08525Japan Society for the Promotion of Science 19K18012JMU Start-Up Grant for Young Investigators
6 · The paper itself

Abstract

AIMS/

introductionImeglimin is a novel oral hypoglycemic agent that improves blood glucose levels through multiple mechanisms of action including the enhancement of glucose-stimulated insulin secretion (GSIS), however, the details of this mechanism have not been clarified. In the process of GSIS, activation of the transient receptor potential melastatin 2 (TRPM2) channel, a type of non-selective cation channel (NSCCs) in β-cells, promotes plasma membrane depolarization. The present study aimed to examine whether imeglimin potentiates GSIS via the TRPM2 channel in β-cells. MATERIALS AND

methodsPancreatic islets were isolated by collagenase digestion from male wild-type and TRPM2-knockout (KO) mice. Insulin release and nicotinamide adenine dinucleotide (NAD

resultsBatch-incubation studies showed that imeglimin enhanced GSIS at stimulatory 16.6 mM glucose, whereas it did not affect basal insulin levels at 2.8 mM glucose. Imeglimin increased the glucose-induced production of NAD

conclusionsImeglimin may activate TRPM2 channels in β-cells via the production of NAD

Indexed as

ADP-ribosyl CyclaseAnimalsBlood GlucoseHypoglycemic AgentsInsulin SecretionIslets of LangerhansMaleMiceSignal TransductionTriazinesTRPM Cation ChannelsADP-ribosyl CyclaseBlood GlucoseHypoglycemic AgentsimegliminTriazinesTRPM2 protein, mouseTRPM Cation ChannelsCyclic ADP riboseImegliminTransient receptor potential melastatin 2

Identifiers

PMID34523242
PMCPMC8756313
OpenAlexW3200098731

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.