Abstract

Type 2 diabetes is characterized by the presence of both fasting and postprandial hyperglycaemia. Glycated haemoglobin is a marker of overall glycaemic exposure and integrates both fasting and postprandial hyperglycaemia. Epidemiologic and interventional studies in type 1 and type 2 diabetes have demonstrated that chronic hyperglycaemia is associated with the appearance of chronic diabetes complications. More importantly, reducing glycated haemoglobin to achieve target goals prevents and avoid progression of complications, in particular microvascular outcomes. Although sustained chronic hyperglycaemia produces excessive protein glycation, acute fluctuations of glucose may activate oxidative stress and contribute to endothelial dysfunction, which may also participate in the development of diabetes complications. Therefore, reducing postprandial hyperglycaemia and glucose variability are now recognised as a priority in treatment of type 2 diabetes. Therapeutic agents acting on postprandial glucose excursions are of particular interest to diminish glucose variability. Emerging therapeutic agents such as the glucagon-like peptide 1 agonists and the dipeptidyl peptidase (DPP)-4 inhibitors are very attractive. Both increase insulin secretion and suppress glucagon release in response to meals, in a glucose-dependent manner. This review will focus on the increasing impact of postprandial hyperglycaemia and glycaemic variability in developing diabetes complications and the role of DPP-4 inhibitors (sitagliptin, vildagliptin, saxagliptin) in reducing both defects presenting in people with type 2 diabetes.

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