Mechanisms of islet amyloidosis toxicity in type 2 diabetes.
Mechanisms of islet amyloidosis toxicity in type 2 diabetes.
复制标题
DOI：
10.1016/j.febslet.2013.01.017
复制
发表时间：
2013-04-17
期刊：
影响因子：
3.5
通讯作者：
Schmidt AM
中科院分区：
文献类型：
--
作者：
Abedini A;Schmidt AM
由神经胰腺激素胰岛淀粉样多肽（IAPP或胰淀素）形成的淀粉样蛋白（amyloid）是已知的最大的淀粉样蛋白生成序列之一，导致2型糖尿病中的胰岛淀粉样变性和胰岛移植失败。在正常情况下，IAPP通过调节几种代谢参数，如饱腹感、血糖水平、肥胖和体重，在维持能量稳态中发挥作用。IAPP淀粉样蛋白形成的机制、IAPP毒性物质的性质以及导致胰腺β细胞毒性的细胞途径尚未得到充分表征。已经提出了几种毒性机制，包括受体和非受体介导的事件。IAPP的类似物已被批准用于治疗糖尿病，并正在研究用于治疗肥胖症。
Amyloid formation by the neuropancreatic hormone, islet amyloid polypeptide (IAPP or amylin), one of the most amyloidogenic sequences known, leads to islet amyloidosis in type 2 diabetes and to islet transplant failure. Under normal conditions, IAPP plays a role in the maintenance of energy homeostasis by regulating several metabolic parameters, such as satiety, blood glucose levels, adiposity and body weight. The mechanisms of IAPP amyloid formation, the nature of IAPP toxic species and the cellular pathways that lead to pancreatic β-cell toxicity are not well characterized. Several mechanisms of toxicity, including receptor and non-receptor-mediated events, have been proposed. Analogs of IAPP have been approved for the treatment of diabetes and are under investigation for the treatment of obesity.