ArticleDiabetologia2019
The role of GIP and pancreatic GLP-1 in the glucoregulatory effect of DPP-4 inhibition in mice.
Article in Diabetologia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Alpha-cell paracrine signaling in the regulation of beta-cell insulin secretion.Frontiers in endocrinology · 2022Review
- Article
- Updating the Role of α-Cell Preproglucagon Products on GLP-1 Receptor-Mediated Insulin Secretion.Diabetes · 2020Article
- Article
- Dipeptidyl Peptidase-IV Inhibitory Activity and Related Molecular Mechanism of Bovine α-Lactalbumin-Derived Peptides.Molecules (Basel, Switzerland) · 2020Article
- Intra-islet GLP-1, but not CCK, is necessary for β-cell function in mouse and human islets.Scientific reports · 2020Article
- Article
- Dipeptidyl Peptidase-4 at the Interface Between Inflammation and Metabolism.Clinical medicine insights. Endocrinology and diabetes · 2020Review
- Communication between the gut microbiota and peripheral nervous system in health and chronic disease.Gut microbesReview
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
aims/hypothesisGlucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are two peptides that function to promote insulin secretion. Dipeptidyl peptidase-4 (DPP-4) inhibitors increase the bioavailability of both GLP-1 and GIP but the dogma continues to be that it is the increase in GLP-1 that contributes to the improved glucose homeostasis. We have previously demonstrated that pancreatic rather than intestinal GLP-1 is necessary for improvements in glucose homeostasis in mice. Therefore, we hypothesise that a combination of pancreatic GLP-1 and GIP is necessary for the full effect of DPP-4 inhibitors on glucose homeostasis.
methodsWe have genetically engineered mouse lines in which the preproglucagon gene (Gcg) is absent in the entire body (GcgRA
resultsAdministration of the DPP-4 inhibitor, linagliptin, improved glucose tolerance in GcgRA CONCLUSIONS/
interpretationTaken together, these data suggest that increases in pancreatic GLP-1 and GIP are necessary for the full effect of DPP-4 inhibitors on glucose tolerance.
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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.