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• W2011751244 abstract "Novel therapeutic strategies for type 2 diabetes are needed, since the current treatment options neither address all pathophysiological mechanisms nor achieve the glycemic target goals. A general islet-cell dysfunction including insulin- and glucagon-secretion defects contributes to the pathophysiology of type 2 diabetes. Improving islet function by incretin hormone action is a novel therapeutic approach. Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are important incretin hormones contributing to 50-70% of the stimulation of insulin secretion after a meal. Dipeptidyl-peptidase IV (DPP-4) inhibitors inhibit the degradation of GLP-1 and GIP as well as that of other regulatory peptides. Sitagliptin, a DPP-4 inhibitor, is orally active and has been shown to be efficacious and safe in clinical studies. Sitagliptin has received approval in Mexico, the United States and other countries. Like other DPP-4 inhibitors, sitagliptin reduces hemoglobin A1c (HbA1c), fasting and postprandial glucose by glucose-dependent stimulation of insulin secretion and inhibition of glucagon secretion. Sitagliptin is weight neutral. Indirect measures show a possible improvement of beta-cell function. Sitagliptin does not cause a higher rate of hypoglycemia in comparison to metformin or placebo. This article gives an overview of the mechanisms of action, pharmacology and clinical trial results of sitagliptin." @default.
• W2011751244 created "2016-06-24" @default.
• W2011751244 creator A5031742996 @default.
• W2011751244 date "2007-01-01" @default.
• W2011751244 modified "2023-10-15" @default.
• W2011751244 title "Sitagliptin: Profile of a novel DPP-4 inhibitor for the treatment of type 2 diabetes (update)" @default.
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• W2011751244 doi "https://doi.org/10.1358/dot.2007.43.11.1157620" @default.
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