ArticleDiabetologia2016
Pancreatic glucose-dependent insulinotropic polypeptide (GIP) (1-30) expression is upregulated in diabetes and PEGylated GIP(1-30) can suppress the progression of low-dose-STZ-induced hyperglycaemia in mice.
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, 27 citations in OpenAlex.
- GLP-1, GIP/GLP-1, and GCGR/GLP-1 receptor agonists: Novel therapeutic agents for metabolic dysfunction-associated steatohepatitis.World journal of gastroenterology · 2024Review
- GLP1-GIP receptor co-agonists: a promising evolution in the treatment of type 2 diabetes.Acta diabetologica · 2024Review
- Tirzepatide, GIP(1-42) and GIP(1-30) display unique signaling profiles at two common GIP receptor variants, E354 and Q354.Frontiers in pharmacology · 2024Article
- Dual GIPR and GLP-1R agonist tirzepatide inhibits aeroallergen-induced allergic airway inflammation in mouse model of obese asthma.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2023Article
- Roles of glucose-dependent insulinotropic polypeptide in diet-induced obesity.Journal of diabetes investigation · 2022Review
- Recent Advances in Incretin-Based Pharmacotherapies for the Treatment of Obesity and Diabetes.Frontiers in endocrinology · 2022Review
- The Role of Incretins on Insulin Function and Glucose Homeostasis.Endocrinology · 2021Review
- Repositioning the Alpha Cell in Postprandial Metabolism.Endocrinology · 2020Review
- Establishment of novel specific assay for short-form glucose-dependent insulinotropic polypeptide and evaluation of its secretion in nondiabetic subjects.Physiological reports · 2020Article
- Article
- A Low-Carbohydrate Diet Improves Glucose Metabolism in Lean Insulinopenic Akita Mice Along With Sodium-Glucose Cotransporter 2 Inhibitor.Frontiers in endocrinology · 2020Article
- Characterisation of Glucose-Dependent Insulinotropic Polypeptide Receptor Antagonists in Rodent Pancreatic Beta Cells and Mice.Clinical medicine insights. Endocrinology and diabetes · 2019Article
- Dipeptidyl peptidase-4 inhibitor treatment induces a greater increase in plasma levels of bioactive GIP than GLP-1 in non-diabetic subjects.Molecular metabolism · 2017Article
- Proteomic profiling of human islets collected from frozen pancreata using laser capture microdissection.Journal of proteomics · 2017Article
- Hypothalamic AMP-Activated Protein Kinase Regulates Biphasic Insulin Secretion from Pancreatic β Cells during Fasting and in Type 2 Diabetes.EBioMedicine · 2016Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisGlucose-dependent insulinotropic polypeptide (GIP) is a peptide hormone released from gut K cells. While the predominant form is GIP(1-42), a shorter form, GIP(1-30), is produced by pancreatic alpha cells and promotes insulin secretion in a paracrine manner. Here, we elucidated whether GIP(1-30) expression is modulated in mouse models of diabetes. We then investigated whether PEGylated GIP(1-30) can improve islet function and morphology as well as suppress the progression to hyperglycaemia in mice treated with low-dose streptozotocin (LD-STZ).
methodsWe examined pancreatic GIP immunoreactivity in rodent diabetic models. We synthesised [D-Ala(2)]GIP(1-30) and modified the C-terminus with polyethylene glycol (PEG) to produce a dipeptidyl peptidase-4 (DPP-4)-resistant long-acting GIP analogue, [D-Ala(2)]GIP(1-30)-PEG. We performed i.p.GTT and immunohistochemical analysis in non-diabetic and LD-STZ diabetic mice, with or without administration of [D-Ala(2)]GIP(1-30)-PEG.
resultsPancreatic GIP expression was concomitantly enhanced with alpha cell expansion in rodent models of diabetes. Treatment with DPP-4 inhibitor decreased both the GIP- and glucagon-positive areas and preserved the insulin-positive area in LD-STZ diabetic mice. Body weight was not affected by [D-Ala(2)]GIP(1-30)-PEG in LD-STZ or non-diabetic mice. Treatment with GIP significantly ameliorated chronic hyperglycaemia and improved glucose excursions in LD-STZ mice. Treatment with GIP also reduced alpha cell expansion in the islets and suppressed plasma glucagon levels compared with non-treated LD-STZ mice. Additionally, [D-Ala(2)]GIP(1-30)-PEG preserved beta cell area via inhibition of apoptosis in LD-STZ mice. CONCLUSIONS/
interpretationOur data suggest that GIP(1-30) expression is upregulated in diabetes, and PEGylated GIP(1-30) can suppress the progression to STZ-induced hyperglycaemia by inhibiting beta cell apoptosis and alpha cell expansion.
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