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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenosine Triphosphate
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Animals
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Diabetes Mellitus, Type 2 / physiopathology*
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Fatty Acids / metabolism
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Gene Expression Regulation
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Glucose / metabolism
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Humans
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Hyperglycemia / physiopathology
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Insulin / metabolism
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Insulin Resistance
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Insulin Secretion
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Ion Channels
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Islets of Langerhans / cytology
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Islets of Langerhans / metabolism
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Islets of Langerhans / physiology*
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Liver / metabolism
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Membrane Transport Proteins / genetics
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Membrane Transport Proteins / metabolism
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Mitochondria / physiology*
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Mitochondrial Proteins / genetics
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Mitochondrial Proteins / metabolism
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Models, Biological
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Muscle, Skeletal / metabolism
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Obesity / physiopathology
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Oxidation-Reduction
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Oxidative Phosphorylation
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Superoxides / metabolism
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Transcription Factors / metabolism
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Uncoupling Protein 2
Substances
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Fatty Acids
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Insulin
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Ion Channels
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Membrane Transport Proteins
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Mitochondrial Proteins
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Transcription Factors
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Uncoupling Protein 2
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peroxisome-proliferator-activated receptor-gamma coactivator-1
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Superoxides
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Adenosine Triphosphate
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Glucose