Incretin physiology and pathophysiology from an A sian perspective

Incretin hormones, such as glucose‐dependent insulinotropic polypeptide and glucagon‐like peptide‐1, are secreted on oral nutrient ingestion and regulate postprandial glucose homeostasis by conveying the signal of intestinal glucose flux. In East Asians, the secretion of glucose‐dependent insulinotropic polypeptide and glucagon‐like peptide‐1 is not reduced in type 2 diabetes relative to normal glucose tolerance. Although the incretin effect is blunted in European patients with type 2 diabetes, a few East Asian studies showed no difference in the incretin effect between type 2 diabetes and normal glucose tolerance. Interestingly, the glucose‐lowering efficacy of dipeptidyl peptidase‐4 inhibitors or glucagon‐like peptide‐1 receptor agonists was reported to be greater in Asians than in non‐Asians. The difference in the treatment responses could be ascribed to a different pathophysiology of type 2 diabetes (lower insulin secretory function and less insulin resistance), lower body mass index, different genetic makeups, preserved incretin effect and different food compositions in East Asians compared with other ethnic groups. Based on the currently available data, incretin‐based therapies appear to be safe and well tolerated in East Asians. Nevertheless, continuous pharmacovigilance is required. The characteristics of incretin biology and treatment responses to incretin‐based therapies should be considered in developing ethnicity‐specific treatment guidelines and making patient‐centered decisions for patients with type 2 diabetes.