Abstract
Several studies have demonstrated that the development of pancreatic islet α- and β-cell dysfunction is pivotal to the onset and progression of hyperglycemia in type 2 diabetes mellitus ( T2DM ).Mealstimulated insulin secretion from β-cell is reduced and fails to meet the demands of the insulin-resistant state.In addition,glucagon production by α-cell,which normally maintains hepatic glucose production during fasting periods,is not suppressed.We all know that islet dysfunction is a critical target for T2DM treatment.lncretin-based therapies,including glucagon-like peptide-1 ( GLP-1 ) receptor agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors,have been shown to be able to restore glucose sensitivity of islet cells and thus improve glycemic control.Nevertheless,their potential impact on islet function in humans remains uncertain and needs further more investigation. Key words: Islet dysfunction; Dipeptidyl peptidase-4 inhibitors ; Diabetes mellitus, type 2
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