Molecular basis of residual feed intake in broilers

Understanding the expression of genes influencing low and high residual feed intake (RFI) is required to elucidate the basic molecular mechanism influencing feed efficiency. Molecular mechanisms affecting RFI are controlled by many factors, such as neural signals, hormones, mitochondrial efficiency, metabolic pathways and nitrogen recycling. This review covers different aspects of molecular mechanisms affecting feed intake, growth and oxidative stress affecting feed efficiency in broilers. Low RFI chickens maintain feed efficiency by reducing feed intake independent of body weight gain, by upregulating CD36, PPARa, HMGCS2 and GCG, and downregulating PCSK2, CALB1, SAT1 and SGK1. Hormones, like cholecystokinin and glucagon, act as an anorexigenic factor, whereas leptin induces feed intake. Various molecular pathways and metabolic signals, such as the central melanocortin system, AMPK pathway, mammalian target of rapamycin (mTOR) pathway and PI3 K/Akt pathway control feed intake by determining the energy status of the body. A major cause of low feed efficiency in broilers is due to the reactive oxygen species-mediated oxidation of protein. Genes related to the ubiquitin-proteasome system such as DERL1, UFD1 L and UFM1 are downregulated in highly feed efficient broilers. In addition, the expression patterns of the genes involved in mitochondrial energy production, such as avANT, COX III, avUCP, iNOS, PPAR2 and avPGC-1a, have been changed, and these can be a marker for selection against lower RFI in chickens.