ArticleProceedings of the National Academy of Sciences of the United States of America1999
Glucose intolerance caused by a defect in the entero-insular axis: a study in gastric inhibitory polypeptide receptor knockout mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00529048 (Quantification of the Incretin Effect in Healthy Subjects and Patients With Type 2 Diabetes Using Increasing Amounts of Oral Glucose Challenges), which is not on this map. Cited by 138 papers.
What it found
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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.
Quantification of the Incretin Effect in Healthy Subjects and Patients With Type 2 Diabetes Using Increasing Amounts of Oral Glucose Challenges
Who cites it
138 citing papers in PubMed, 453 citations in OpenAlex.
- The dipeptidyl peptidase-4 inhibitor sitagliptin improves vascular endothelial function in type 2 diabetes.Journal of Korean medical science · 2012Trial
- Rapid tachyphylaxis of the glucagon-like peptide 1-induced deceleration of gastric emptying in humans.Diabetes · 2011Trial
- The influence of hepatic impairment on the pharmacokinetics of the dipeptidyl peptidase IV (DPP-4) inhibitor vildagliptin.European journal of clinical pharmacology · 2007Trial
- Glycemic and bodyweight effects ofScience advances · 2026Article
- Clinical Potential of GIP in Type 2 Diabetes and Obesity.Diabetes care · 2026Review
- Endogenous GIP signaling is indispensable for DPP-4 inhibitor-mediated metabolic control in mice.Journal of diabetes investigation · 2026Article
- A metabolic comparison of GIPR agonism versus GIPR antagonism in male mice.Diabetes, obesity & metabolism · 2026Article
- Glucagon-like peptide-1 receptor signaling deficiency exacerbates hematopoietic stem cell graft rejection in mice.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- GPCR Biased Signaling in Metabolism.Handbook of experimental pharmacology · 2026Review
- Acute exogenous acyl-GIP treatment enhances lipid handling and fatty acid oxidation by involving brown fat.EMBO reports · 2025Article
- Physiology and clinical applications of GIP.Endocrine journal · 2025Review
- The Premise of the Paradox: Examining the Evidence That Motivated GIPR Agonist and Antagonist Drug Development Programs.Journal of clinical medicine · 2025Review
- Article
- Evaluating glucose-dependent insulinotropic polypeptide and glucagon as key regulators of insulin secretion in the pancreatic islet.American journal of physiology. Endocrinology and metabolism · 2024Review
- Incretin hormones and pharmacomimetics rapidly inhibit AgRP neuron activity to suppress appetite.bioRxiv : the preprint server for biology · 2024Article
- Dietary impact on fasting and stimulated GLP-1 secretion in different metabolic conditions - a narrative review.The American journal of clinical nutrition · 2024Review
- Review
- Advances in the Management of Diabetes and Overweight using Incretin-based Pharmacotherapies.Current diabetes reviews · 2024Review
- Gastric inhibitory polypeptide receptor antagonism suppresses intramuscular adipose tissue accumulation and ameliorates sarcopenia.Journal of cachexia, sarcopenia and muscle · 2023Article
- Relevance and consequence of chronic inflammation for obesity development.Molecular and cellular pediatrics · 2023Review
78 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mice with a targeted mutation of the gastric inhibitory polypeptide (GIP) receptor gene (GIPR) were generated to determine the role of GIP as a mediator of signals from the gut to pancreatic beta cells. GIPR-/- mice have higher blood glucose levels with impaired initial insulin response after oral glucose load. Although blood glucose levels after meal ingestion are not increased by high-fat diet in GIPR+/+ mice because of compensatory higher insulin secretion, they are significantly increased in GIPR-/- mice because of the lack of such enhancement. Accordingly, early insulin secretion mediated by GIP determines glucose tolerance after oral glucose load in vivo, and because GIP plays an important role in the compensatory enhancement of insulin secretion produced by a high insulin demand, a defect in this entero-insular axis may contribute to the pathogenesis of diabetes.
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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 OpenQuestion graph.