Evidence map›Paper›PMID 12410638›Full record

ArticleThe Biochemical journal2003

Glucagon-like peptide-1 mobilizes intracellular Ca2+ and stimulates mitochondrial ATP synthesis in pancreatic MIN6 beta-cells.

Takashi Tsuboi, Gabriela da Silva Xavier, George G Holz, Laurence S Jouaville, Andrew P Thomas, Guy A Rutter

Open access · greenAbstract read
In one paragraph

Article in The Biochemical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
14.0field-weighted citation impact, top 1% 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

85 citing papers in PubMed, 210 citations in OpenAlex.

  1. Article
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  5. Review
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  15. Review
  16. The therapeutic potential of GLP-1 receptor biased agonism.British journal of pharmacology · 2022 · on this map
    Review
  17. The Pancreatic β-Cell: The Perfect Redox System.Antioxidants (Basel, Switzerland) · 2021
    Review
  18. Article
  19. Glucagon-like peptide 1 (GLP-1).Molecular metabolism · 2019 · on this map
    Review
  20. Article

25 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Takashi TsuboiHenry Wellcome Laboratories for Integrated Cell Signalling, Department of Biochemistry, School of Medical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, U.K.
Gabriela da Silva Xavier
George G Holz
Laurence S Jouaville
Andrew P Thomas
Guy A Rutter
New York University · US

Funding

Insulinotropin: A Modulator Of B-Cell Glucose SignalingR01DK045817 · NIDDK · UPSTATE MEDICAL UNIVERSITY · PI HOLZ, GEORGE G · 2001 to 2008
$3.0M
Diabetes UK 13/0004672NIDDK NIH HHS R01 DK045817
6 · The paper itself

Abstract

Glucagon-like peptide-1 (GLP-1) is a potent regulator of glucose-stimulated insulin secretion whose mechanisms of action are only partly understood. In the present paper, we show that at low (3 mM) glucose concentrations, GLP-1 increases the free intramitochondrial concentrations of both Ca(2+) ([Ca(2+)](m)), and ATP ([ATP](m)) in clonal MIN6 beta-cells. Suggesting that cAMP-mediated release of Ca(2+) from intracellular stores is responsible for these effects, increases in [ATP](m) that were induced by GLP-1 were completely blocked by the Rp isomer of adenosine-3',5'-cyclic monophosphothioate (Rp-cAMPS), or by chelation of intracellular Ca(2+). Furthermore, inhibition of Ins(1,4,5) P (3) (IP(3)) receptors with xestospongin C, or application of ryanodine, partially inhibited GLP-1-induced [ATP](m) increases, and the simultaneous blockade of both IP(3) and ryanodine receptors (RyR) completely eliminated the rise in [ATP](m). GLP-1 appeared to prompt Ca(2+)-induced Ca(2+) release through IP(3) receptors via a protein kinase A (PKA)-mediated phosphorylation event, since ryanodine-insensitive [ATP](m) increases were abrogated with the PKA inhibitor, H89. In contrast, the effects of GLP-1 on RyR-mediated [ATP](m) increases were apparently mediated by the cAMP-regulated guanine nucleotide exchange factor cAMP-GEFII, since xestospongin C-insensitive [ATP](m) increases were blocked by a dominant-negative form of cAMP-GEFII (G114E,G422D). Taken together, these results demonstrate that GLP-1 potentiates glucose-stimulated insulin release in part via the mobilization of intracellular Ca(2+), and the stimulation of mitochondrial ATP synthesis.

Indexed as

Adenosine TriphosphateAnimalsCalciumCalcium SignalingCarbacholCell LineChelating AgentsCholinergic AgonistsColforsinCyclic AMPDiazoxideEgtazic AcidEnzyme InhibitorsGlucagonGlucagon-Like Peptide 1Glucoseadenosine-3',5'-cyclic phosphorothioateAdenosine TriphosphateCalciumCarbacholChelating AgentsCholinergic AgonistsColforsinCyclic AMPDiazoxideEgtazic AcidEnzyme InhibitorsGlucagonGlucagon-Like Peptide 1GlucoseInsulinMacrocyclic CompoundsOxazolesPeptide FragmentsProtein PrecursorsRyanodineRyanodine Receptor Calcium Release ChannelThionucleotidesxestospongin A

Identifiers

PMID12410638
PMCPMC1223096
OpenAlexW2110160705

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.