Evidence map›Paper›PMID 24843552›Full record

ReviewJournal of diabetes investigation2012

Glucose-dependent insulinotropic polypeptide signaling in pancreatic β-cells and adipocytes.

Christopher Hs McIntosh, Scott Widenmaier, Su-Jin Kim

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of diabetes investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

23 citing papers in PubMed, 56 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
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  7. Review
  8. Mechanisms of action of incretin receptor based dual- and tri-agonists in pancreatic islets.American journal of physiology. Endocrinology and metabolism · 2023
    Review
  9. G protein-coupled receptors and obesity.Frontiers in endocrinology · 2023
    Review
  10. Article
  11. Article
  12. The Pancreatic β-Cell: The Perfect Redox System.Antioxidants (Basel, Switzerland) · 2021
    Review
  13. Article
  14. Article
  15. Incretins in obesity and diabetes.Annals of the New York Academy of Sciences · 2020
    Review
  16. Review
  17. Article
  18. Article
  19. Fatty Acid-Stimulated Insulin Secretion vs. Lipotoxicity.Molecules (Basel, Switzerland) · 2018
    Review
  20. 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

3 authors at 2 institutions in 2 countries.

Christopher Hs McIntoshDepartment of Cellular and Physiological Sciences and the Diabetes Research Group, Life Sciences Institute University of British Columbia, Vancouver, BC, Canada.
Scott WidenmaierDepartment of Cellular and Physiological Sciences and the Diabetes Research Group, Life Sciences Institute University of British Columbia, Vancouver, BC, Canada.
Su-Jin KimDepartment of Cellular and Physiological Sciences and the Diabetes Research Group, Life Sciences Institute University of British Columbia, Vancouver, BC, Canada.
Harvard University · USUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucose-dependent insulinotropic polypeptide (GIP) was the first incretin to be identified. In addition to stimulating insulin secretion, GIP plays regulatory roles in the maintenance, growth and survival of pancreatic islets, as well as impacting on adipocyte function. The current review focuses on the intracellular signaling pathways by which GIP contributes to the regulation of β-cell secretion and survival, and adipocyte differentiation and lipogenesis. Studies on signaling underlying the insulinotropic actions of the incretin hormones have largely been carried out with glucagon-like peptide-1. They have provided evidence for contributions by both protein kinase A (PKA) and exchange protein directly activated by cyclic adenosine monophosphate (EPAC2), and their probable role in GIP signaling is discussed. Recent studies have shown that inhibition of the kinase apoptosis signal-regulating kinase 1 (ASK1) by GIP plays a key role in reducing mitochondria-induced apoptosis in β-cells through protein kinase B (PKB)-mediated pathways, and that GIP-induced post-translational modification of voltage- dependent K(+) (Kv) channels also contributes to its prosurvival role. Through regulation of gene expression, GIP tips the balance between pro- and anti-apoptotic members of the B-cell lymphoma-2 (Bcl-2) protein family towards β-cell survival. GIP also plays important roles in the differentiation of pre-adipocytes to adipocytes, and in the regulation of lipoprotein lipase expression and lipogenesis. These events involve interactions between GIP, insulin and resistin signaling pathways. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2012.00196.x, 2012).

Indexed as

ApoptosisGlucose‐dependent insulinotropic polypeptideIncretin

Identifiers

PMID24843552
PMCPMC4020726
OpenAlexW2153248040

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.