Mitochondrial Dysfunction and Type 2 Diabetes

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 {szligbeta} cells. Defects in the former are responsible for insulin resistance, and defects in the latter...

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Veröffentlicht in:	Science (American Association for the Advancement of Science) 2005-01, Vol.307 (5708), p.384-387
Hauptverfasser:	Lowell, Bradford B, Shulman, Gerald I
Format:	Artikel
Sprache:	eng
Schlagworte:	Adenosine Triphosphate Animals B lymphocytes Biological and medical sciences Care and treatment Causes of Cellular biology Delta cells Development and progression Diabetes Diabetes Mellitus, Type 2 - physiopathology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Evidence Fatty acids Fatty Acids - metabolism Gene Expression Regulation Glucose Glucose - metabolism Health aspects Hispanic Americans Humans Hyperglycemia Hyperglycemia - physiopathology Inhibition Insulin Insulin - metabolism Insulin Resistance Insulin Secretion Ion Channels Islets of Langerhans - cytology Islets of Langerhans - metabolism Islets of Langerhans - physiology Liver - metabolism Medical research Medical sciences Membrane Transport Proteins - genetics Membrane Transport Proteins - metabolism Metabolism Mitochondria - physiology Mitochondrial diseases Mitochondrial Proteins - genetics Mitochondrial Proteins - metabolism Models, Biological Muscle, Skeletal - metabolism Obesity Obesity - physiopathology Oxidation-Reduction Oxidative Phosphorylation Superoxides - metabolism Transcription Factors - metabolism Type 1 diabetes mellitus Type 2 diabetes Type 2 diabetes mellitus Uncoupling Protein 2 Viewpoints
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Beschreibung
Zusammenfassung:	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 {szligbeta} 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.
ISSN:	0036-8075 1095-9203
DOI:	10.1126/science.1104343