Duodenal mitochondrial function and feed efficiency in broilers

Studies were conducted to evaluate the potential link between intestinal mitochondrial function and biochemistry with the phenotypic expression of feed efficiency (FE) in a single line of broilers. Duodenal mitochondria isolated from low FE birds provided with FADH2-linked substrate had lower respiratory chain coupling, whereas oxidative phosphorylation capability was either equal or superior to that in mitochondria from broilers with high FE. Mitochondria from low FE birds exhibited greater electron leak, apparently from site-specific defects at Complex I and II of the electron transport chain. Addition of a chemical uncoupler (FCCP) lowered H2O2 production in mitochondria from low FE broilers suggesting that uncoupling oxidative phosphorylation may be a compensatory mechanism to lower H 2O2 production in these birds. Respiratory chain complex activities, except for Complex IV (cytochrome c oxidase), were lower in mitochondria from low FE birds. The GSSG/GSH ratio was higher (P = 0.07) in mitochondria from low FE broilers, indicating higher oxidative stress. This concurs with observations of higher H2 O2 production and higher protein carbonyls (oxidation) in mitochondria from low FE birds that in turn may cause differential expression of mitochondrial genes and proteins. Protein expression studies showed that 6 of 7 nuclear-encoded protein subunits (70S[FP], core I, core II, cyt c1, ISP and ATPase-alpha) were higher while 3 of 6 mitochondrial-encoded subunits (ND4, ND6-C, COX II) were lower in the low compared to the high FE group. Real-time PCR analysis showed that mRNA expression of inducible nitric oxide synthase and peroxisome proliferator-activated receptor-gamma (PPAR-gamma) were lower in the duodenum of low FE broilers, with no differences in avian adenine nucleotide translocase, COX III and PPAR-gamma co-activator 1-alpha between groups. To our knowledge, these studies are the first to demonstrate biochemical differences in mitochondria isolated from small intestines of broilers with low and high FE. Future studies could investigate upstream signals or key cellular pathways while a more global look at differences in expression of mitochondrial proteins and/or genes between high and low FE birds could be exploited to develop FE biomarker(s) to aid selection programs in identifying breeder replacement stock with inferior or superior FE.