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Superoxide Production by Rat Skeletal Muscle Mitochondria: Influence of High Fat Diet
Author(s) -
Glancy Brian,
Willis Wayne
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.126
Subject(s) - oligomycin , superoxide , mitochondrion , skeletal muscle , chemistry , medicine , reactive oxygen species , endocrinology , respiration , glycolysis , biochemistry , biology , metabolism , anatomy , enzyme , atpase
Chronic positive energy and fat balances increase the risk for the development of skeletal muscle insulin resistance. Reactive oxygen species may be a consequence and/or a contributing factor to this pathology. The purpose of this study was to evaluate superoxide (O 2 .) production by mitochondria (MITO) isolated from gastrocnemius muscle of rats fed standard chow (C) or a high fat (HF) diet. MITO were respired under either a static condition (oligomycin, OLIGO) or at an experimentally established ATP free energy corresponding to about 50% of maximal respiration (flow condition). Respiratory substrates were provided at saturating concentrations and O 2 . production was followed. Under the OLIGO condition MITO oxidizing pyruvate + malate (P+M) generated very low rates of O 2 . production irrespective of diet. In contrast, P+M supplemented with the cytosolic‐mitochondrial electron shuttle substrates glycerol‐3‐phosphate and glutamate elicited O 2 . generation rates severalfold greater than P+M alone. Moreover, MITO from HF animals produced much higher O 2 . production than C rats when these products of the glycolytic pathway were available as respiratory fuels. For both C and HF MITO, the flow condition drastically reduced O 2 . production for all fuels and combinations. These findings suggest that excessive fuel and carbohydrate availability under sedentary conditions may promote the generation of reactive oxygen species. Supported by NSF IBN‐0116997