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炎症介质与胰岛β细胞功能衰竭:1型糖尿病与2型糖尿病之间的联系。

Inflammatory mediators and islet beta-cell failure: a link between type 1 and type 2 diabetes.

作者信息

Donath Marc Y, Størling Joachim, Maedler Kathrin, Mandrup-Poulsen Thomas

机构信息

Division of Endocrinology and Diabetes, University Hospital, 8091 Zurich, Switzerland.

出版信息

J Mol Med (Berl). 2003 Aug;81(8):455-70. doi: 10.1007/s00109-003-0450-y. Epub 2003 Jul 18.

DOI:10.1007/s00109-003-0450-y
PMID:12879149
Abstract

Pancreatic islet beta-cell death occurs in type 1 and 2 diabetes mellitus, leading to absolute or relative insulin deficiency. beta-cell death in type 1 diabetes is due predominantly to autoimmunity. In type 2 diabetes beta-cell death occurs as the combined consequence of increased circulating glucose and saturated fatty acids together with adipocyte secreted factors and chronic activation of the innate immune system. In both diabetes types intra-islet inflammatory mediators seem to trigger a final common pathway leading to beta-cell apoptosis. Therefore anti-inflammatory therapeutic approaches designed to block beta-cell apoptosis could be a significant new development in type 1 and 2 diabetes.

摘要

1型和2型糖尿病均会发生胰岛β细胞死亡,导致绝对或相对的胰岛素缺乏。1型糖尿病中的β细胞死亡主要归因于自身免疫。在2型糖尿病中,β细胞死亡是循环葡萄糖和饱和脂肪酸增加,以及脂肪细胞分泌因子和先天免疫系统慢性激活共同作用的结果。在两种类型的糖尿病中,胰岛内的炎症介质似乎都会触发导致β细胞凋亡的最终共同途径。因此,旨在阻止β细胞凋亡的抗炎治疗方法可能成为1型和2型糖尿病治疗的重大新进展。

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