Modulation of redox state in pigs differeing in feed efficiency as revealed by a proteomic analysis

High-yielding dairy cows enter a negative energy balance after calving because feed intake is too low to meet the energy requirements for maintenance and milk production. At this time, cows mobilize their fat reserves – a process that is thought to interfere with the increase of feed intake. The control of feed intake results from the integration of humoral and nerval signals at feed intake regulatory centers in the brain. Metabolic oxidation in peripheral organs, primarily in the liver, may activate nerval signaling which is integrated and translated into anorexic responses by neurons of the hypothalamus (Ht). To study the relationship between metabolic oxidation and feed intake, cows were kept in respiration chambers with simultaneous recording of gas exchange and feed intake. All feed intake events were strongly cross-correlated with carbohydrate and fat oxidation in late-lactating cows. Transition cows with higher fat mobilization capacity (H cows) exhibited the greater fat oxidation, accompanied by the greater expression of hepatic enzymes involved in various fatty acid oxidation pathways and oxidative phosphorylation, each before and after parturition. H cows revealed greater plasma acyl ghrelin concentrations and the higher acyl:total ghrelin ratio, before and after parturition. The acyl:total ghrelin ratio correlated with several aspects of fat metabolism, but not with feed intake, implying that the ghrelin system plays a prominent role in fat allocation and oxidation rather than exerting orexigenic effects. Also, H cows had less activated orexigenic neurons in the arcuate nucleus of the Ht as indicated by the lower percentage of cFOS activated agouti-related protein (AgRP) neurons. Differential AgRP neuron activation was not associated with feed intake but with decreased oxygen consumption, increased respiratory quotient, and reduced NEFA concentrations, suggesting that AgRP activation plays a pivotal role in the regulation of metabolic oxidation during early lactation.