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J Diabetes Investig. 2015;6(5):495-507.

Incretin physiology and pathophysiology from an Asian perspective.

제1저자 조영민 · 교신저자 조영민

PMID 26417406 PMC4578486 DOI 10.1111/jdi.12305 IF 3.6 내분비대사내과
소속 (1)
  1. Department of Internal Medicine, Seoul National University College of Medicine Seoul, Korea.

Abstract

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.

Keywords

AsianIncretinType 2 diabetes mellitus

Figures

Figure 1
Figure 1 A comparison of insulin secretion and insulin sensitivity between East Asians and Northern Europeans. The disposition index (DI) was calculated by the product of insulinogenic index (an index of insulin secretion) and the Matsuda index (an index of insulin sensitivity during an oral glucose tolerance test). The dotted lines represent hyperbolic curves of the designated DI of 110 (for normal glucose tolerance [NGT]), 50 (for impaired glucose tolerance [IGT]) and 20 (for type 2 diabetes mellitus [T2DM]). The approximate positions of each circle are drawn based on the data presented by Møller et al.18
Figure 2
Figure 2 Components contributing to the incretin effect and the gastrointestinally-mediated glucose disposal (GIGD). Whereas the incretin effect reflects only the insulin secretory function of pancreatic β-cells, the GIGD represents all of the components, including β-cells, α-cells, liver, gut and other visceral organs, skeletal muscle, and fat, in regulating the postprandial glucose metabolism. GIP, glucose-dependent insulinotropic polypeptide; GLP-1, glucagon-like peptide-1; HGP, hepatic glucose production.
Figure 3
Figure 3 The theoretical glucose-lowering effects of therapies augmenting insulin secretion according to the different baseline insulin secretion and insulin sensitivity. This figure is drawn with an assumption that the same amount of insulin secretion occurred in East Asians and Northern Europeans with type 2 diabetes shown in Figure 1. The areas of the rectangles (the product of insulin secretion and insulin sensitivity) represent the theoretical glucose-lowering effects in the two ethnic groups with type 2 diabetes (T2DM).

그림 출처: PubMed Central 공개 논문 (PMC4578486)

그 밖의 정보
출판 형태
Journal Article, Review
저널
Journal of diabetes investigation · ISSN 2040-1116
전자 출판
2014-12-17
참고문헌
91편