线粒体功能障碍与2型糖尿病

Mitochondrial dysfunction and type 2 diabetes.

作者信息

Lowell Bradford B, Shulman Gerald I

机构信息

Department of Medicine, Beth Israel Deaconess Medical Center, 99 Brookline Avenue, Harvard Medical School, Boston, MA 02215, USA.

出版信息

Science. 2005 Jan 21;307(5708):384-7. doi: 10.1126/science.1104343.

DOI:10.1126/science.1104343

PMID:15662004

Abstract

Maintenance of normal blood glucose levels depends on a complex interplay between the insulin responsiveness of skeletal muscle and liver and glucose-stimulated insulin secretion by pancreatic beta cells. Defects in the former are responsible for insulin resistance, and defects in the latter are responsible for progression to hyperglycemia. Emerging evidence supports the potentially unifying hypothesis that both of these prominent features of type 2 diabetes are caused by mitochondrial dysfunction.

摘要

正常血糖水平的维持取决于骨骼肌和肝脏的胰岛素反应性与胰腺β细胞的葡萄糖刺激胰岛素分泌之间的复杂相互作用。前者的缺陷导致胰岛素抵抗，后者的缺陷导致进展为高血糖。新出现的证据支持这一潜在的统一假说，即2型糖尿病的这两个突出特征均由线粒体功能障碍引起。