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The influence of dietary lipids on mitochondrial hydrogen peroxide production in skeletal muscle of calorie restricted mice
Author(s) -
Chen Yana,
Hagopian Kevork,
Ramsey Jon
Publication year - 2011
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.25.1_supplement.lb79
Subject(s) - skeletal muscle , mitochondrion , reactive oxygen species , chemistry , lipid oxidation , biochemistry , hydrogen peroxide , medicine , inner mitochondrial membrane , oxidative phosphorylation , calorie restriction , oxidative stress , endocrinology , food science , lipid peroxide , biology , antioxidant , lipid peroxidation
Calorie restriction (CR) has been shown to reduce reactive oxygen species (ROS) production, attenuate oxidative damage and retard aging in a variety of species. Interestingly, CR has been reported to alter membrane composition towards saturation. This has led to a theory that changes in membrane saturation are central to the actions of CR. As a first step towards testing this theory, C57BL/6 mice were assigned to 4 dietary groups (control and three CR groups) and fed AIN‐93G diets at either 95% (control) or 60% (CR) of ad libitum. To manipulate membrane composition, the primary dietary fats for the CR groups were soybean oil (also used in the control diet), fish oil or lard. The diets were fed for 1 month and then mitochondria from hindlimb skeletal muscle were isolated for measures of mitochondrial lipid composition, proton leak, and H 2 O 2 production. Results indicate that changes in mitochondrial lipids in the CR mice reflected the dietary lipid sources. Mitochondrial H 2 O 2 production was decreased ( P <0.02) in all three CR groups compared to the control group regardless of the substrate used for respiration. However, there was no evidence of difference when comparisons were between CR groups. The results of this study indicate that an increased degree of saturation in mitochondrial membranes is not required for reduced ROS production with CR in muscle. (Supported by NIH RO1 AG028125)