Islet Inflammation Impairs the Pancreatic β-Cell in Type 2 Diabetes

被引：267

作者：

Donath, Marc Y. ^{[1
]}

Boeni-Schnetzler, Marianne

Ellingsgaard, Helga

Ehses, Jan A.

机构：

[1] Univ Zurich Hosp, Div Endocrinol Diabet & Nutr, CH-8091 Zurich, Switzerland

来源：

PHYSIOLOGY | 2009年 / 24卷 / 06期

关键词：

STIMULATED-INSULIN-SECRETION; SATURATED FATTY-ACIDS; ADIPOSE-TISSUE; OXIDATIVE STRESS; KAPPA-B; GK RAT; GLUCOSE; EXPRESSION; RESISTANCE; OBESITY;

D O I：

10.1152/physiol.00032.2009

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

Onset of Type 2 diabetes occurs when the pancreatic beta-cell fails to adapt to the increased insulin demand caused by insulin resistance. Morphological and therapeutic intervention studies have uncovered an inflammatory process in islets of patients with Type 2 diabetes characterized by the presence of cytokines, immune cells, beta-cell apoptosis, amyloid deposits, and fibrosis. This insulitis is due to a pathological activation of the innate immune system by metabolic stress and governed by IL-1 signaling. We propose that this insulitis contributes to the decrease in beta-cell mass and the impaired insulin secretion observed in patients with Type 2 diabetes.

引用

页码：325 / 331

页数：7

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