Evidence map›Paper›PMID 33782700›Full record

ReviewEndocrinology2021

The Role of Incretins on Insulin Function and Glucose Homeostasis.

Jens Juul Holst, Lærke Smidt Gasbjerg, Mette Marie Rosenkilde

Open access · hybridAbstract readReview
In one paragraph

Review in Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
12.0field-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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Jens Juul HolstDepartment of Biomedical Sciences and the NovoNordisk Center for Basic Metabolic Research, Faculty of Health Sciences, University of Copenhagen, The Panum Institute, Copenhagen N, DK-2200Denmark.ORCID 0000-0001-6853-3805
Lærke Smidt GasbjergDepartment of Biomedical Sciences and the NovoNordisk Center for Basic Metabolic Research, Faculty of Health Sciences, University of Copenhagen, The Panum Institute, Copenhagen N, DK-2200Denmark.ORCID 0000-0002-7880-8515
Mette Marie RosenkildeDepartment of Biomedical Sciences and the NovoNordisk Center for Basic Metabolic Research, Faculty of Health Sciences, University of Copenhagen, The Panum Institute, Copenhagen N, DK-2200Denmark.ORCID 0000-0001-9600-3254
University of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incretin effect-the amplification of insulin secretion after oral vs intravenous administration of glucose as a mean to improve glucose tolerance-was suspected even before insulin was discovered, and today we know that the effect is due to the secretion of 2 insulinotropic peptides, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1). But how important is it? Physiological experiments have shown that, because of the incretin effect, we can ingest increasing amounts of amounts of glucose (carbohydrates) without increasing postprandial glucose excursions, which otherwise might have severe consequences. The mechanism behind this is incretin-stimulated insulin secretion. The availability of antagonists for GLP-1 and most recently also for GIP has made it possible to directly estimate the individual contributions to postprandial insulin secretion of a) glucose itself: 26%; b) GIP: 45%; and c) GLP-1: 29%. Thus, in healthy individuals, GIP is the champion. When the action of both incretins is prevented, glucose tolerance is pathologically impaired. Thus, after 100 years of research, we now know that insulinotropic hormones from the gut are indispensable for normal glucose tolerance. The loss of the incretin effect in type 2 diabetes, therefore, contributes greatly to the impaired postprandial glucose control.

Indexed as

Blood GlucoseDiabetes Mellitus, Type 2Gastric Inhibitory PolypeptideGlucagon-Like Peptide 1HomeostasisHumansIncretinsInsulinInsulin SecretionPostprandial PeriodReceptors, Gastrointestinal HormoneBlood GlucoseGastric Inhibitory Polypeptidegastric inhibitory polypeptide receptorGlucagon-Like Peptide 1IncretinsInsulinReceptors, Gastrointestinal Hormoneexendin 9-39glucagon-like peptide-1 (GLP-1)glucose-dependent insulinotropic polypeptide (GIP)hormone antagonistshormone coagonists

Identifiers

PMID33782700
PMCPMC8168943
OpenAlexW3139973230

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.