Evidence map›Paper›PMID 23077547›Full record

ArticlePloS one2012

Glucose decouples intracellular Ca2+ activity from glucagon secretion in mouse pancreatic islet alpha-cells.

Sylvain J Le Marchand, David W Piston

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 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  7. Article
  8. Metabolic regulation of glucagon secretion.The Journal of endocrinology · 2023
    Article
  9. Review
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  13. Review
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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

2 authors at 1 institution in 1 country.

Sylvain J Le MarchandDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, USA.
David W Piston
Vanderbilt University · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
DYNAMICS OF PANCREATIC ISLET FUNCTIONR01DK053434 · NIDDK · VANDERBILT UNIVERSITY · PI PISTON, DAVID W · 1998 to 2010
$3.1M
Probes:Quantitative Optical and Electron Microscopy(RMI)P20GM072048 · NIGMS · VANDERBILT UNIVERSITY · PI PISTON, DAVID W. · 2004 to 2007
$2.7M
Multi-Function Laser Scanning MicroscopeS10RR025649 · NCRR · VANDERBILT UNIVERSITY · PI PISTON, DAVID W · 2009 to 2009
$499k
NCI NIH HHS CA68485NCI NIH HHS P30 CA068485NCRR NIH HHS RR25649NCRR NIH HHS S10 RR025649NIDDK NIH HHS DK20593NIDDK NIH HHS DK53434NIDDK NIH HHS DK58404NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK053434NIGMS NIH HHS GM72048NIGMS NIH HHS P20 GM072048
6 · The paper itself

Abstract

The mechanisms of glucagon secretion and its suppression by glucose are presently unknown. This study investigates the relationship between intracellular calcium levels ([Ca(2+)](i)) and hormone secretion under low and high glucose conditions. We examined the effects of modulating ion channel activities on [Ca(2+)](i) and hormone secretion from ex vivo mouse pancreatic islets. Glucagon-secreting α-cells were unambiguously identified by cell specific expression of fluorescent proteins. We found that activation of L-type voltage-gated calcium channels is critical for α-cell calcium oscillations and glucagon secretion at low glucose levels. Calcium channel activation depends on K(ATP) channel activity but not on tetrodotoxin-sensitive Na(+) channels. The use of glucagon secretagogues reveals a positive correlation between α-cell [Ca(2+)](i) and secretion at low glucose levels. Glucose elevation suppresses glucagon secretion even after treatment with secretagogues. Importantly, this inhibition is not mediated by K(ATP) channel activity or reduction in α-cell [Ca(2+)](i). Our results demonstrate that glucose uncouples the positive relationship between [Ca(2+)](i) and secretory activity. We conclude that glucose suppression of glucagon secretion is not mediated by inactivation of calcium channels, but instead, it requires a calcium-independent inhibitory pathway.

Indexed as

AnimalsArginineCalciumCalcium SignalingGlucagonGlucagon-Secreting CellsGlucoseMiceMice, Inbred C57BLMice, TransgenicPotassium ChannelsSodium Channel BlockersSodium ChannelsTetrodotoxinArginineCalciumGlucagonGlucosePotassium ChannelsSodium Channel BlockersSodium ChannelsTetrodotoxin

Identifiers

PMID23077547
PMCPMC3471958
OpenAlexW2162936216

What OpenQuestion holds

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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.