Evidence map›Paper›PMID 31785304›Full record

ReviewPeptides2020

The role of GIP in α-cells and glucagon secretion.

Kimberley El, Jonathan E Campbell

Open access · greenAbstract readReview
In one paragraph

Review in Peptides, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
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  11. Effects of Glucagon-Like Peptide-1 Receptor Agonists (Mono and Combination Therapy) on Energy Expenditure: A Scoping Review.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Article
  12. Article
  13. Circulating levels of gut hormones in anorexia nervosa before and after short-term weight restoration.Progress in neuro-psychopharmacology & biological psychiatry · 2026
    Article
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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.

Kimberley ElDuke Molecular Physiology Institute, USA.
Jonathan E CampbellDuke Molecular Physiology Institute, USA; Department of Medicine, Division of Endocrinology, Duke University, Durham, NC, USA; Department of Pharmacology and Cancer Biology, Duke University, Durham, NC, USA. Electronic address: jonathan.campbell@duke.edu.
Duke University · US

Funding

Endocrinology and Metabolism Training ProgramT32DK007012 · NIDDK · DUKE UNIVERSITY · PI DAVID A. D'ALESSIO · 1986 to 2026
$6.8M
Novel metabolic actions of GIPR01DK125353 · NIDDK · DUKE UNIVERSITY · PI CAMPBELL, JONATHAN E, D'ALESSIO, DAVID A. · 2020 to 2024
$2.1M
Mechanisms of insulin secretion mediated by alpha cellsR01DK123075 · NIDDK · DUKE UNIVERSITY · PI CAMPBELL, JONATHAN E · 2019 to 2023
$1.9M
NIDDK NIH HHS R01 DK123075NIDDK NIH HHS R01 DK125353NIDDK NIH HHS T32 DK007012
6 · The paper itself

Abstract

Glucose-dependent insulinotropic polypeptide (GIP) is an intestinally derived peptide that is secreted in response to feeding. The GIP receptor (GIPR) is expressed in many cell types involved in the regulation of metabolism, including α- and β-cells. Glucagon and insulin exert tremendous control over glucose metabolism. Thus, GIP action in islets strongly dictates metabolic control in the postprandial state. Loss of GIPR activity in β-cells is a characteristic of type 2 diabetes (T2D) which associates with reduced postprandial insulin secretion and hyperglycemia. Less is known about GIPR activity in α-cells or the control of glucagon secretion. GIP stimulates glucagon secretion in a glucose-dependent manner in healthy people, with enhanced activity at lower glycemia. However, GIP stimulates glucagon secretion even at hyperglycemia in people with T2D, suggesting that inappropriate GIPR activity in α-cells contributes to the pathogenesis of T2D. Here, we review the literature describing GIP action and GIPR activity in the α-cell, detailing the basic science that has shaped the view of how GIP regulates glucagon secretion. We also contrast the effects of GIP on glucagon secretion in healthy and T2D people. Finally, we contextualize these observations in light of recent work that redefines the role of glucagon in glucose homeostasis, suggesting that hyperglucagonemia per se does not drive hyperglycemia. As new medications for T2D that incorporate GIPR activity are being developed, it is clear that a better understanding of GIPR activity beyond the β-cell is necessary. This work highlights the importance of focusing on the GIPR in α-cells.

Indexed as

AnimalsDiabetes Mellitus, Type 2Gastric Inhibitory PolypeptideGastrointestinal AgentsGlucagonGlucagon-Secreting CellsHumansInsulin-Secreting CellsReceptors, Gastrointestinal HormoneGastric Inhibitory Polypeptidegastric inhibitory polypeptide receptorGastrointestinal AgentsGlucagonReceptors, Gastrointestinal HormoneAlpha cellDiabetesGlucose-dependent insulinotropic polypeptideIncretin

Identifiers

PMID31785304
PMCPMC7580028
OpenAlexW2990930253

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.