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东亚人2型糖尿病发病机制中的β细胞功能障碍与胰岛素抵抗

β cell dysfunction versus insulin resistance in the pathogenesis of type 2 diabetes in East Asians.

作者信息

Yabe Daisuke, Seino Yutaka, Fukushima Mitsuo, Seino Susumu

机构信息

Center for Diabetes, Endocrinology and Metabolism, Kansai Electric Power Hospital, 2-1-7 Fukushima-ku, Osaka, 553-0003, Japan,

出版信息

Curr Diab Rep. 2015 Jun;15(6):602. doi: 10.1007/s11892-015-0602-9.

DOI:10.1007/s11892-015-0602-9
PMID:25944304
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4420838/
Abstract

Type 2 diabetes (T2DM) is one of the most serious global health problems and is mainly a result of the drastic increase in East Asia, which includes over a fourth of the global diabetes population. Lifestyle factors and ethnicity are two determinants in the etiology of T2DM, and lifestyle changes such as higher fat intake and less physical activity link readily to T2DM in East Asians. It is widely recognized that T2DM in East Asians is characterized primarily by β cell dysfunction, which is evident immediately after ingestion of glucose or meal, and less adiposity compared to the disease in Caucasians. These pathophysiological differences have an important impact on therapeutic approaches. Here, we revisit the pathogenesis of T2DM in light of β cell dysfunction versus insulin resistance in East Asians and discuss ethnic differences in the contributions of insulin secretion and insulin resistance, together with incretin secretin and action, to glucose intolerance.

摘要

2型糖尿病(T2DM)是最严重的全球健康问题之一,主要是由于东亚地区的急剧增加所致,该地区占全球糖尿病人口的四分之一以上。生活方式因素和种族是T2DM病因的两个决定因素,而高脂肪摄入和较少体育活动等生活方式的改变与东亚人的T2DM密切相关。人们普遍认识到,东亚人的T2DM主要特征是β细胞功能障碍,这在摄入葡萄糖或进食后立即明显,并且与白种人中的该疾病相比肥胖程度较低。这些病理生理差异对治疗方法有重要影响。在此,我们根据东亚人β细胞功能障碍与胰岛素抵抗重新审视T2DM的发病机制,并讨论胰岛素分泌和胰岛素抵抗以及肠促胰岛素分泌和作用对葡萄糖不耐受的贡献中的种族差异。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b0e/4420838/43c9e0c58f38/11892_2015_602_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b0e/4420838/43c9e0c58f38/11892_2015_602_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b0e/4420838/43c9e0c58f38/11892_2015_602_Fig1_HTML.jpg

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