Evidence map›Paper›PMID 20921208›Full record

ArticleDiabetes2011

Lack of TRPM2 impaired insulin secretion and glucose metabolisms in mice.

Kunitoshi Uchida, Katsuya Dezaki, Boldbaatar Damdindorj, Hitoshi Inada, Tetsuya Shiuchi, Yasuo Mori, Toshihiko Yada, Yasuhiko Minokoshi, Makoto Tominaga

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 3% 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

90 citing papers in PubMed, 1 synthesis or guideline pooled it, 182 citations in OpenAlex.

  1. Pooled it
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  9. A conserved mechanism couples cytosolic domain movements to pore gating in the TRPM2 channel.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. TRPM channels in health and disease.Nature reviews. Nephrology · 2024
    Review
  11. Article
  12. Article
  13. TRPC3 Regulates Islet Beta-Cell Insulin Secretion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
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30 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Kunitoshi UchidaNational Institutes of Natural Sciences, Okazaki, Japan.
Katsuya Dezaki
Boldbaatar Damdindorj
Hitoshi Inada
Tetsuya Shiuchi
Yasuo Mori
Toshihiko Yada
Yasuhiko Minokoshi
Makoto Tominaga
Jichi Medical University · JPThe Graduate University for Advanced Studies, SOKENDAI · JPNational Institute for Physiological Sciences · JPKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTRPM2 is a Ca²(+)-permeable nonselective cation channel activated by adenosine dinucleotides. We previously demonstrated that TRPM2 is activated by coapplication of heat and intracellular cyclic adenosine 5'-diphosphoribose, which has been suggested to be involved in intracellular Ca²(+) increase in immunocytes and pancreatic β-cells. To clarify the involvement of TRPM2 in insulin secretion, we analyzed TRPM2 knockout (TRPM2-KO) mice. RESEARCH DESIGN AND

methodsOral and intraperitoneal glucose tolerance tests (OGTT and IPGTT) were performed in TRPM2-KO and wild-type mice. We also measured cytosolic free Ca²(+) in single pancreatic cells using fura-2 microfluorometry and insulin secretion from pancreatic islets.

resultsBasal blood glucose levels were higher in TRPM2-KO mice than in wild-type mice without any difference in plasma insulin levels. The OGTT and IPGTT demonstrated that blood glucose levels in TRPM2-KO mice were higher than those in wild-type mice, which was associated with an impairment in insulin secretion. In isolated β-cells, smaller intracellular Ca²(+) increase was observed in response to high concentrations of glucose and incretin hormone in TRPM2-KO cells than in wild-type cells. Moreover, insulin secretion from the islets of TRPM2-KO mice in response to glucose and incretin hormone treatment was impaired, whereas the response to tolbutamide, an ATP-sensitive potassium channel inhibitor, was not different between the two groups.

conclusionsThese results indicate that TRPM2 is involved in insulin secretion stimulated by glucose and that further potentiated by incretins. Thus, TRPM2 may be a new target for diabetes therapy.

Indexed as

AnimalsBlood GlucoseCalciumGlucose Tolerance TestHot TemperatureInsulinInsulin SecretionIslets of LangerhansMaleMiceMice, KnockoutTRPM Cation ChannelsBlood GlucoseCalciumInsulinTRPM2 protein, mouseTRPM Cation Channels

Identifiers

PMID20921208
PMCPMC3012163
OpenAlexW2125984333

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.