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Glucose-dependent insulinotropic polypeptide receptor signaling alleviates gut inflammation in mice.
JCI Insight
December 2024
Lunenfeld-Tanenbaum Research Institute, Sinai Health System, University of Toronto, Toronto, Canada.
Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are gut-derived peptide hormones that potentiate glucose-dependent insulin secretion. The clinical development of GIP receptor (GIPR)-GLP-1 receptor (GLP-1R) multi-agonists exemplified by tirzepatide and emerging GIPR antagonist-GLP-1R agonist therapeutics such as maritide is increasing interest in the extra-pancreatic actions of incretin therapies. Both GLP-1 and GIP modulate inflammation, with GLP-1 also acting locally to alleviate gut inflammation in part through anti-inflammatory actions on GLP-1R+ intestinal intraepithelial lymphocytes.
View Article and Find Full Text PDFPancreatic Safety of Tirzepatide and Its Effects on Islet Cell Function: A Systematic Review and Meta-Analysis.
Obes Sci Pract
December 2024
Background: Endogenous glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) regulate islet cell function. GLP-1 receptor agonists (GLP-1RAs) have been associated with an elevated risk of acute pancreatitis. Data on the pancreatic safety of tirzepatide (a dual GLP-1 and GIP agonist) and its effects on islet cell function in randomized controlled trials (RCTs) are scarce.
View Article and Find Full Text PDFIdentifying the Role of Individual Seal IAPP Amino Acids in Inhibiting the Aggregation of Human IAPP.
Protein Pept Lett
December 2024
Department of Chemistry and Biochemistry, Loyola Marymount University, 1 LMU Drive, Los Angeles, CA90045, USA.
Introduction: The progression of type 2 diabetes in humans appears to be linked to the loss of insulin-producing β-cells. One of the major contributors to β-cell loss is the formation of toxic human IAPP amyloid (hIAPP, Islet Amyloid Polypeptide, amylin) in the pancreas. Inhibiting the formation of toxic hIAPP amyloid could slow, if not prevent altogether, the progression of type 2 diabetes.
View Article and Find Full Text PDFGalNT2-mediated O-glycosylation affects pancreas development and function in mice.
Sci Rep
November 2024
Department of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, 20246, Hamburg, Germany.
GALNT2, also known as polypeptide N-acetylgalactosaminyltransferase 2, is an enzyme that catalyzes the initial step of O-linked glycosylation, a crucial posttranslational modification that affects protein folding, stability, and function. Alterations in GALNT2 activity have been implicated in various diseases, such as cancer, metabolic disorders, and cardiovascular diseases, highlighting its importance in maintaining normal physiological functions. To investigate the impact of GalNT2 overexpression in vivo for the first time, we generated a conditional transgenic mouse line in which GalNT2 was expressed specifically in the pancreas.
View Article and Find Full Text PDFDoes Incretin Agonism Have Sustainable Efficacy?
Cells
November 2024
Lunenfeld-Tanenbaum Research Institute, Sinai Health System, Toronto, ON M5T 3L9, Canada.
Recent clinical trials using synthetic incretin hormones, glucagon-like peptide 1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP) receptor agonists have demonstrated that these treatments ameliorated many complications related to obesity, emphasizing the significant impact of body weight on overall health. Incretins are enteroendocrine hormones secreted by gut endothelial cells triggered by nutrient ingestion. The phenomenon that oral ingestion of glucose elicits a much higher insulin secretion than intra-venous injection of equimolar glucose is known as the incretin effect.
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