Mitochondrial Dysfunction and Type 2 Diabetes

Author:

Lowell Bradford B.12,Shulman Gerald I.12

Affiliation:

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

2. Howard Hughes Medical Institute, Department of Internal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06536, USA.

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 β 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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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