肠促胰岛素
内科学
内分泌学
胃抑制多肽
胰岛素
葡萄糖稳态
激素
分泌物
胰高血糖素样肽-1
肠内分泌细胞
受体
餐后
胰高血糖素
胃肠激素
生物
化学
肽类激素
2型糖尿病
胰岛素抵抗
医学
糖尿病
内分泌系统
出处
期刊:PubMed
日期:1995-12-01
卷期号:21 (5): 311-8
被引量:46
摘要
Although glucose is the major regulator of insulin secretion by pancreatic beta cells, its action is modulated by several neural and hormonal stimuli. In particular, hormones secreted by intestinal endocrine cells stimulate glucose-induced insulin secretion very potently after nutrient absorption. These hormones, called gluco-incretins or insulinotropic hormones, are major regulators of postprandial glucose homeostasis. The main gluco-incretins are GIP (gastric inhibitory polypeptide or glucose-dependent insulinotropic polypeptide) and GLP-1 (glucagon-like polypeptide-1). The secretion of GIP, a 42 amino acid polypeptide secreted by duodenal K cells, is triggered by fat and glucose. GIP stimulation of insulin secretion depends on the presence of specific beta-cell receptors and requires glucose at a concentration at least equal to or higher than the normoglycaemic level of approximately 5 mM. GIP accounts for about 50% of incretin activity, and the rest may be due to GLP-1 which is produced by proteolytic processing of the preproglucagon molecule in intestinal L cells. GLP-1 is the most potent gluco-incretin characterized so far. As with GIP, its stimulatory action requires a specific membrane receptor and normal or elevated glucose concentrations. Contrary to GIP, the incretin effect of GLP-1 is maintained in non-insulin-dependent diabetic patients. This peptide or agonists of its beta-cell receptor could provide new therapeutic tools for the treatment of Type II diabetic hyperglycaemia.
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