Evidence map›Paper›PMID 21220323›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Augmented glucose-induced insulin release in mice lacking G(o2), but not G(o1) or G(i) proteins.

Ying Wang, Sangeun Park, Neil S Bajpayee, Yoshiko Nagaoka, Guylain Boulay, Lutz Birnbaumer, Meisheng Jiang

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. GFrontiers in aging neuroscience · 2019
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Insulin secretion stimulated by L-arginine and its metabolite L-ornithine depends on Gα(i2).American journal of physiology. Endocrinology and metabolism · 2014
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Go2 G protein mediates galanin inhibitory effects on insulin release from pancreatic β cells.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  17. 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

7 authors at 3 institutions in 1 country.

Ying WangDepartment of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Sangeun Park
Neil S Bajpayee
Yoshiko Nagaoka
Guylain Boulay
Lutz Birnbaumer
Meisheng Jiang
University of California, Los Angeles · USNational Institute of Environmental Health Sciences · USNational Institutes of Health · US

Funding

Transmembrane Signaling MechanismsZIAES101643 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRNBAUMER, LUTZ · 2011 to 2014
$5.4M
Transmembrane Signaling MechanismsZ01ES101643 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRNBAUMER, LUTZ · 2003 to 2008
$5.1M
Transmembrane Signaling Mechanisms Involving TRP ChannelsZIAES101684 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRNBAUMER, LUTZ · 2011 to 2014
$3.2M
Modulation of Insulin Secretion via Go2 G-ProteinR01DK069771 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI JIANG, MEISHENG · 2005 to 2009
$1.6M
Intramural NIH HHS Z01 ES101643NIDDK NIH HHS DK 069771NIDDK NIH HHS DK19319NIDDK NIH HHS R01 DK069771
6 · The paper itself

Abstract

Insulin secretion by pancreatic β cells is a complex and highly regulated process. Disruption of this process can lead to diabetes mellitus. One of the various pathways involved in the regulation of insulin secretion is the activation of heterotrimeric G proteins. Bordetella pertussis toxin (PTX) promotes insulin secretion, suggesting the involvement of one or more of three G(i) and/or two G(o) proteins as suppressors of insulin secretion from β cells. However, neither the mechanism of this inhibitory modulation of insulin secretion nor the identity of the G(i/o) proteins involved has been elucidated. Here we show that one of the two splice variants of G(o), G(o2), is a key player in the control of glucose-induced insulin secretion by β cells. Mice lacking G(o2)α, but not those lacking α subunits of either G(o1) or any G(i) proteins, handle glucose loads more efficiently than wild-type (WT) mice, and do so by increased glucose-induced insulin secretion. We thus provide unique genetic evidence that the G(o2) protein is a transducer in an inhibitory pathway that prevents damaging oversecretion of insulin.

Indexed as

AnimalsBlotting, WesternBrainFemaleGene ExpressionGlucoseGlucose Tolerance TestGTP-Binding Protein alpha Subunits, Gi-GoImmunohistochemistryInsulinInsulin SecretionIn Vitro TechniquesIslets of LangerhansMaleMiceMice, Inbred C57BLGlucoseGTP-Binding Protein alpha Subunits, Gi-GoInsulinProtein Isoforms

Identifiers

PMID21220323
PMCPMC3029743
OpenAlexW2047967291

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.