Evidence map›Paper›PMID 17498508›Full record

ReviewGastroenterology2007

Biology of incretins: GLP-1 and GIP.

Laurie L Baggio, Daniel J Drucker

2 registry-linked trialsAbstract readReview
PubMed Publisher
In one paragraph

Review in Gastroenterology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 1,455 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,455citing papers in PubMed, 8 pooled it
71.6field-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.

NCT06243536 phase4unknown statusstarted 2024, after this paper: background citation

The Effect of Semaglutide on Disordered Eating Behaviour in Type 2 Diabetic Patients

Ran2024Enrolled60Registered outcomes3Posted comparisons0ConditionsDisordered Eating Behaviors, Overweight, Type 2 DiabetesArmssemaglutide, Standard of care
PMID 27208320PMID 25870084PMID 36722623PMID 25330463PMID 25745131PMID 24245943PMID 21157325PMID 19336687PMID 16682865PMID 11728508PMID 26301188PMID 27443001other papers from this trial
Open the trial in the graph
NCT02324010 phase2completednot on this mapstarted 2015, after this paper: background citation

Effects of Sitagliptin on Postprandial Glycaemia, Incretin Hormones and Blood Pressure in Type 2 Diabetes - Relationship to Gastric Emptying

TypeinterventionalSponsorRoyal Adelaide HospitalRan2015 to 2017Enrolled14ConditionsGastroparesis, Diabetes MellitusArmsSitagliptin, Placebo
3 · Its place in the literature

Who cites it

1,455 citing papers in PubMed, 8 syntheses or guidelines pooled it, 3,531 citations in OpenAlex.

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  5. New Perspectives in Modulating the Entero-Insular Axis in Pediatric Obesity.International journal of molecular sciences · 2025
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  12. GLP-1 in patients with myocardial infarction complicated by cardiogenic shock-an IABP-SHOCK II-substudy.Clinical research in cardiology : official journal of the German Cardiac Society · 2024
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1,395 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

2 authors at 2 institutions in 1 country.

Laurie L BaggioDepartment of Medicine, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Banting and Best Diabetes Centre, University of Toronto, Toronto, Ontario, Canada.
Daniel J Drucker
Mount Sinai Hospital · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This review focuses on the mechanisms regulating the synthesis, secretion, biological actions, and therapeutic relevance of the incretin peptides glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). The published literature was reviewed, with emphasis on recent advances in our understanding of the biology of GIP and GLP-1. GIP and GLP-1 are both secreted within minutes of nutrient ingestion and facilitate the rapid disposal of ingested nutrients. Both peptides share common actions on islet beta-cells acting through structurally distinct yet related receptors. Incretin-receptor activation leads to glucose-dependent insulin secretion, induction of beta-cell proliferation, and enhanced resistance to apoptosis. GIP also promotes energy storage via direct actions on adipose tissue, and enhances bone formation via stimulation of osteoblast proliferation and inhibition of apoptosis. In contrast, GLP-1 exerts glucoregulatory actions via slowing of gastric emptying and glucose-dependent inhibition of glucagon secretion. GLP-1 also promotes satiety and sustained GLP-1-receptor activation is associated with weight loss in both preclinical and clinical studies. The rapid degradation of both GIP and GLP-1 by the enzyme dipeptidyl peptidase-4 has led to the development of degradation-resistant GLP-1-receptor agonists and dipeptidyl peptidase-4 inhibitors for the treatment of type 2 diabetes. These agents decrease hemoglobin A1c (HbA1c) safely without weight gain in subjects with type 2 diabetes. GLP-1 and GIP integrate nutrient-derived signals to control food intake, energy absorption, and assimilation. Recently approved therapeutic agents based on potentiation of incretin action provide new physiologically based approaches for the treatment of type 2 diabetes.

Indexed as

AnimalsClinical Trials as TopicDiabetes Mellitus, Type 2Gastric Inhibitory PolypeptideGastrointestinal HormonesGlucagon-Like Peptide 1Glycated HemoglobinHemoglobinsHumansInsulin-Secreting CellsReceptors, GlucagonSignal TransductionGastric Inhibitory PolypeptideGastrointestinal HormonesGlucagon-Like Peptide 1Glycated Hemoglobinhemoglobin A1c protein, humanHemoglobinsReceptors, Glucagon

Identifiers

PMID17498508
OpenAlexW2084948079

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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.