Role of Mitochondria in the Phenotypic Expression of Feed Efficiency

Recent investigations were conducted on mitochondria obtained from broilers with low and high feed efficiency (FE) within the same genetic line that were fed the same diet, thereby allowing relationships between mitochondrial function and the phenotypic expression of FE to be clearly established. In these studies, breast muscle, liver and duodenal mitochondria obtained from broilers with high FE exhibited a more tightly coupled respiratory chain along with lower electron leak and reactive oxygen species (ROS) production compared with broilers with low FE. Elevated electron leak in low FE was due to site-specific defects in electron transport at Complex I, III, or both of the respiratory chains in breast and leg muscles and at Complex I, II, or III (depending on energy substrate) in duodenal mitochondria. Increased ROS production was presumably responsible for increased protein oxidation in low FE muscle mitochondria. Of 14 respiratory chain proteins investigated in breast muscle, the expression of 4 (3 in Complex III and 1 in Complex IV) was higher in low FE mitochondria. Interestingly, low FE was associated with a general suppression in respiratory chain complex activities (I, II, III, and IV) in breast muscle and liver. Elucidation of the mechanisms responsible for lower ROS production and tighter coupling of the respiratory chain in high FE mitochondria will greatly facilitate our understanding of the cellular basis for the phenotypic expression of FE.