Incretins and the development of type 2 diabetes.
Incretins and the development of type 2 diabetes.
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DOI：
10.1007/s11892-006-0034-7
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发表时间：
2006-06-01
影响因子：
4.2
通讯作者：
Nauck, Michael A
中科院分区：
文献类型：
--
作者：
Meier, Juris J;Nauck, Michael A
肠促胰岛素激素胃抑制多肽（GIP）和胰高血糖素样肽1（GLP-1）响应营养摄入而释放，并增强胰腺β细胞葡萄糖刺激的胰岛素分泌。这种胃肠激素增加餐后胰岛素分泌的作用称为肠促胰岛素效应。2型糖尿病患者中肠促胰岛素的作用几乎完全不存在。这是由于1）餐后GLP-1分泌减少约15%和2）GIP的促胰岛素活性几乎完全丧失。这篇综述文章总结了2型糖尿病患者以及高危人群中GIP和GLP-1分泌异常和促胰岛素作用的临床研究。一个显着比例的一级亲属的特点是减少促胰岛素反应外源性GIP。然而，这种现象不会使葡萄糖耐量更快地恶化或转化为葡萄糖耐量受损或糖尿病。因此，虽然有迹象表明，早期异常肠促胰岛素分泌和行动在糖尿病前期人群，它还没有被证明，这种现象是2型糖尿病的发病机制的核心。
The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are released in response to nutrient ingestion and potentiate glucose-stimulated insulin secretion from pancreatic beta cells. The augmentation of postprandial insulin secretion by such gastrointestinal hormones is called the incretin effect. The incretin effect is almost completely absent in patients with type 2 diabetes. This is due to 1) an approximate 15% reduction in postprandial GLP-1 secretion and 2) a near total loss of insulinotropic activity of GIP. This review article summarizes clinical studies on abnormalities in the secretion and insulinotropic effects of GIP and GLP-1 in patients with type 2 diabetes as well as in individuals at high risk. A significant proportion of first-degree relatives are characterized by a reduced insulinotropic response to exogenous GIP. Nevertheless, this phenomenon does not predispose to a more rapid deterioration in glucose tolerance or conversion to impaired glucose tolerance or diabetes. Therefore, although there are hints of early abnormalities in incretin secretion and action in prediabetic populations, it has not been proven that such phenomena are central to the pathogenesis of type 2 diabetes.