ArticleDiabetologia2016
Endogenous GIP ameliorates impairment of insulin secretion in proglucagon-deficient mice under moderate beta cell damage induced by streptozotocin.
Article in Diabetologia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Adrenal hormones in the maintenance of glucose homeostasis during prolonged fasting in male glucagon-deficient mice.Journal of diabetes investigation · 2026Article
- Acute high-protein feeding induces hepatic amino acid accumulation in diabetic male mice prior to transcriptional adaptation.Physiological reports · 2026Article
- Effects of MCC950 on lipid profiles, glycemic control, and sympathetic dysfunction in a streptozotocin-induced type 1 diabetic rat model.Croatian medical journal · 2026Article
- A DYRK inhibitor ameliorates glucose homeostasis and increases incretin-producing cells in diabetic mice.Journal of molecular endocrinology · 2026Article
- Impaired Fat Absorption from Intestinal Tract in High-Fat Diet Fed Male Mice Deficient in Proglucagon-Derived Peptides.Nutrients · 2024Article
- 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
- Advances in basic research on glucagon and alpha cells.Diabetology international · 2024Review
- Tirzepatide's innovative applications in the management of type 2 diabetes and its future prospects in cardiovascular health.Frontiers in pharmacology · 2024Review
- Blockade of glucagon increases muscle mass and alters fiber type composition in mice deficient in proglucagon-derived peptides.Journal of diabetes investigation · 2023Article
- Roles of glucose-dependent insulinotropic polypeptide in diet-induced obesity.Journal of diabetes investigation · 2022Review
- High Protein Diet Feeding Aggravates Hyperaminoacidemia in Mice Deficient in Proglucagon-Derived Peptides.Nutrients · 2022Article
- Functional adenosine triphosphate-sensitive potassium channel is required in high-carbohydrate diet-induced increase in β-cell mass.Journal of diabetes investigation · 2019Article
- Regulation of amino acid metabolism and α-cell proliferation by glucagon.Journal of diabetes investigation · 2018Review
- Incretin concept revised: The origin of the insulinotropic function of glucagon-like peptide-1 - the gut, the islets or both?Journal of diabetes investigation · 2018Article
- The dual DPP4 inhibitor and GPR119 agonist HBK001 regulates glycemic control and beta cell function ex and in vivo.Scientific reports · 2017Article
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Authors and funding
17 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisThe action of incretin hormones including glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) is potentiated in animal models defective in glucagon action. It has been reported that such animal models maintain normoglycaemia under streptozotocin (STZ)-induced beta cell damage. However, the role of GIP in regulation of glucose metabolism under a combination of glucagon deficiency and STZ-induced beta cell damage has not been fully explored.
methodsIn this study, we investigated glucose metabolism in mice deficient in proglucagon-derived peptides (PGDPs)-namely glucagon gene knockout (GcgKO) mice-administered with STZ. Single high-dose STZ (200 mg/kg, hSTZ) or moderate-dose STZ for five consecutive days (50 mg/kg × 5, mSTZ) was administered to GcgKO mice. The contribution of GIP to glucose metabolism in GcgKO mice was also investigated by experiments employing dipeptidyl peptidase IV (DPP4) inhibitor (DPP4i) or Gcg-Gipr double knockout (DKO) mice.
resultsGcgKO mice developed severe diabetes by hSTZ administration despite the absence of glucagon. Administration of mSTZ decreased pancreatic insulin content to 18.8 ± 3.4 (%) in GcgKO mice, but ad libitum-fed blood glucose levels did not significantly increase. Glucose-induced insulin secretion was marginally impaired in mSTZ-treated GcgKO mice but was abolished in mSTZ-treated DKO mice. Although GcgKO mice lack GLP-1, treatment with DPP4i potentiated glucose-induced insulin secretion and ameliorated glucose intolerance in mSTZ-treated GcgKO mice, but did not increase beta cell area or significantly reduce apoptotic cells in islets. CONCLUSIONS/
interpretationThese results indicate that GIP has the potential to ameliorate glucose intolerance even under STZ-induced beta cell damage by increasing insulin secretion rather than by promoting beta cell survival.
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