Feeding regime alters mitochondrial metabolism in beef skeletal muscle

Le résumé fourni par la source

Plane of nutrition influences animal growth rate and muscle fiber composition, potentially through altering skeletal muscle metabolism. The objective of this study was to evaluate changes in skeletal muscle metabolism in response to altering diet without changes in growth rate. To that end, cattle were fed high-concentrate diets typically used in commercial feedlots until they reached market weight, approximately 604 kg. Cattle were then placed on isocaloric, maintenance diets consisting of primarily grain and forage diets for 60 d until harvest. Cattle fed a forage-based maintenance diet had increased mitochondrial succinate dehydrogenase (SDHA, P < 0.05), citrate synthase (CS, P < 0.01), electron transport chain complex I (CI, P < 0.01), complex II (CII, P < 0.01), and voltage dependent anion channel (VDAC, P < 0.001) protein abundances. Mitochondrial oxygen consumption rate was greatest in muscle mitochondria of forage-fed cattle when provided glutamate/malate (P < 0.05), acetoacetate/malate (P < 0.01), and palmitoyl-carnitine/malate (P < 0.05). This increased function is partially explained by increases in the abundance of electron transport chain complexes and the voltage-gated dependent anion channel (VDAC, P < 0.01), the pore allowing ATP to leave the mitochondria. Significant interaction between diet and muscle were noted for ACSS1 (P < 0.01) gene expressions. Additionally, forage-maintained cattle had increased ACSS1 (P < 0.01), CPT1b (P < 0.05), and CPT2 (P < 0.05) gene expression when compared to grain-maintained cattle. These data suggest part of the mechanism responsible for altered mitochondrial function in response to altered substrate availability may lie in the regulation of ACSS1, CPT1b, and CPT2 gene expressions for acetate and fatty acid metabolism. Together, diet influences muscle acetate and fatty acid gene expressions, mitochondrial protein abundances, and mitochondrial function in fatty acid substrate oxidation, highlighting the role of nutrition on skeletal muscle metabolism and possibly as a means of regulating tissue growth.

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