Evidence map›Paper›PMID 22761801›Full record

ArticlePloS one2012

Mice deficient in GEM GTPase show abnormal glucose homeostasis due to defects in beta-cell calcium handling.

Jenny E Gunton, Mary Sisavanh, Rebecca A Stokes, Jon Satin, Leslie S Satin, Min Zhang, Sue M Liu, Weikang Cai, Kim Cheng, Gregory J Cooney and 7 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
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

17 authors at 9 institutions in 2 countries.

Jenny E GuntonDiabetes and Transcription Factors Group, Garvan Institute of Medical Research, Sydney, Australia. j.gunton@garvan.org.au
Mary Sisavanh
Rebecca A Stokes
Jon Satin
Leslie S Satin
Min Zhang
Sue M Liu
Weikang Cai
Kim Cheng
Gregory J Cooney
D Ross Laybutt
Trina So
Juan-Carlos Molero
Shane T Grey
Douglas A Andres
Michael S Rolph
Charles R Mackay
Garvan Institute of Medical Research · AUUniversity of Kentucky · USGriffith University · AUMichigan United · USMonash University · AUSt Vincent's Clinic · AUUNSW Sydney · AUVirginia Commonwealth University · USWestmead Hospital · AU

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
METABOLICALLY-COUPLED ION CHANNEL INTERACTIONS IN ISLETSR01DK046409 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI SATIN, LESLIE S. · 1994 to 2023
$9.1M
Mechanisms of Long-term Cardiac Ion Channel RegulationR01HL074091 · NHLBI · UNIVERSITY OF KENTUCKY · PI SATIN, JONATHAN · 2003 to 2013
$3.3M
Regulation of Calcium Channel Function by the Rem GTPaseR01HL072936 · NHLBI · UNIVERSITY OF KENTUCKY · PI ANDRES, DOUGLAS ALLEN, SATIN, JONATHAN · 2003 to 2013
$3.0M
Medical Research CouncilNHLBI NIH HHS R01 HL072936NHLBI NIH HHS R01 HL074091NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK046409NIDDK NIH HHS R01 DK46409
6 · The paper itself

Abstract

aims and hypothesisGlucose-stimulated insulin secretion from beta-cells is a tightly regulated process that requires calcium flux to trigger exocytosis of insulin-containing vesicles. Regulation of calcium handling in beta-cells remains incompletely understood. Gem, a member of the RGK (Rad/Gem/Kir) family regulates calcium channel handling in other cell types, and Gem over-expression inhibits insulin release in insulin-secreting Min6 cells. The aim of this study was to explore the role of Gem in insulin secretion. We hypothesised that Gem may regulate insulin secretion and thus affect glucose tolerance in vivo.

methodsGem-deficient mice were generated and their metabolic phenotype characterised by in vivo testing of glucose tolerance, insulin tolerance and insulin secretion. Calcium flux was measured in isolated islets.

resultsGem-deficient mice were glucose intolerant and had impaired glucose stimulated insulin secretion. Furthermore, the islets of Gem-deficient mice exhibited decreased free calcium responses to glucose and the calcium oscillations seen upon glucose stimulation were smaller in amplitude and had a reduced frequency.

conclusionsThese results suggest that Gem plays an important role in normal beta-cell function by regulation of calcium signalling.

Indexed as

AnimalsCalciumCalcium SignalingGlucoseGlucose IntoleranceInsulinInsulin ResistanceInsulin-Secreting CellsInsulin SecretionMiceMice, KnockoutMonomeric GTP-Binding ProteinsCalciumGem protein, mouseGlucoseInsulinMonomeric GTP-Binding Proteins

Identifiers

PMID22761801
PMCPMC3386271
OpenAlexW2117693733

What OpenQuestion holds

Textmetadata
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.