DECREASE OF STIMULATED AMYLIN RELEASE PRECEDES IMPAIRMENT OF INSULIN-SECRETION IN TYPE-II DIABETES
DECREASE OF STIMULATED AMYLIN RELEASE PRECEDES IMPAIRMENT OF INSULIN-SECRETION IN TYPE-II DIABETES
复制标题
DOI：
10.2337/diabetes.40.12.1615
复制
发表时间：
1991-12-01
期刊：
影响因子：
7.7
通讯作者：
PRAGER, R
中科院分区：
文献类型：
--
作者：
LUDVIK, B;LELL, B;PRAGER, R
胰淀素是一种由37个氨基酸组成的多肽，已被鉴定为非胰岛素依赖型（II型）糖尿病患者胰腺淀粉样蛋白沉积物的主要蛋白质组分。 胰淀素与胰岛素一起储存和释放，并且已经提出在II型糖尿病的发病机制中起主要作用。 为了比较不同代谢条件下胰淀素释放及其与胰岛素分泌的比例，在健康、瘦对照受试者、具有正常和受损葡萄糖耐量（分别为NGT和IGT）的肥胖患者和肥胖II型糖尿病患者中进行口服和静脉内葡萄糖耐量试验（分别为OGTT和IVGTT）。 与对照组相比，OGTT期间基础和刺激胰淀素分泌在NGT和IGT的肥胖患者中显着较高，但在II型糖尿病患者中没有。 NGT肥胖患者的胰淀素反应显著高于瘦对照组和肥胖程度匹配的II型糖尿病患者。 糖耐量异常和糖耐量异常的肥胖患者的淀粉样蛋白-胰岛素比值略有下降，而II型糖尿病患者的淀粉样蛋白-胰岛素比值则显著下降。 胰淀素的分泌显着刺激IVGTT期间在对照组和肥胖患者NGT和IGT，但不是在II型糖尿病患者。 这些发现表明，胰淀素在非糖尿病受试者中以恒定的胰岛素比例由胰腺β细胞生理性释放。 糖耐量异常和糖耐量异常的肥胖受试者中葡萄糖刺激的胰淀素分泌增加。 在II型糖尿病中，胰淀素分泌相对于胰岛素分泌减少，并且胰淀素不被IVGTT刺激。
Amylin, a 37-amino acid polypeptide, has been identified as the major protein component of pancreatic amyloid deposits in patients with non-insulin-dependent (type II) diabetes mellitus. Amylin is stored and released together with insulin and has been proposed to play a major role in the pathogenesis of type II diabetes. To compare amylin release and its proportion to insulin secretion under different metabolic conditions, oral and intravenous glucose tolerance tests (OGTT and IVGTT, respectively) were performed in healthy, lean control subjects, obese patients with normal and impaired glucose tolerance (NGT and IGT, respectively), and obese type II diabetic patients. Compared with control subjects, basal and stimulated amylin secretion during OGTT was significantly higher in obese patients with NGT and IGT but not in type II diabetic patients. The integrated amylin response was significantly higher in obese patients with NGT than lean control subjects and type II diabetic patients matched for degree of obesity. The amylin-insulin ratio decreased slightly in obese subjects with NGT and IGT and significantly in type II diabetic patients. Amylin secretion was significantly stimulated during IVGTT in control subjects and obese patients with NGT and IGT but not in type II diabetic patients. These findings suggest that amylin is physiologically released by pancreatic beta-cells in a constant ratio to insulin in nondiabetic subjects. Glucose-stimulated amylin secretion is increased in obese subjects with NGT and IGT. In type II diabetes mellitus, amylin secretion relative to that of insulin is decreased, and amylin is not stimulated by IVGTT.