Physiological Mechanisms Controlling Feeding Behavior
Mechanisms controlling feed intake are dependent upon the interaction between diet and physiological state of animals. Physiological state is affected by age, pregnancy, lactation, and adiposity and is characterized by differences in insulin sensitivity of tissues and plasma concentrations of insulin, growth hormone, and leptin. The interaction between diet and physiological state affects feeding behavior (e.g. meal size and frequency) depending upon the type and temporal supply of absorbed fuels. These fuels (e.g. glucose, fatty acids, amino acids) derive from the diet directly or indirectly as a result of gastrointestinal fermentation and are metabolized or stored by different tissues at different rates. Other fuels (e.g. long chain fatty acids, glycerol, amino acids) originate from body reserves. Effects of fuels on endocrine response and gene expression affect energy partitioning, which in turn affects feeding behavior by altering clearance of fuels from the blood. Various signals are integrated in brain feeding centers and dominant mechanisms controlling feed intake change with physiological state. Signals that affect feeding behavior include those from gut distension, which likely dominates control of feed intake under conditions of high-energy requirements with low-energy diets, as well as those from the release of gut peptides stimulated by certain nutrients. There is a growing consensus of the importance of fuel-based sensing among tissues. Signals to brain feeding centers via hepatic vagal afferents are also affected by oxidation of fuels. While oxidation of fuels has been linked to feeding behavior, evidence suggests that the mechanism is specifically related to hepatic energy charge (degree of phosphorylation of adenine nucleotides). Synergistic effects of metabolic inhibitors have been demonstrated in rodents, which suggests an integrated mechanism with a common signal related to hepatic energy status from oxidation of a variety of fuels. Utilization of high-energy phosphate bonds vary with liver function and their production is determined by the flux of carbon through acetyl CoA and activity of the tricarboxylic acid cycle. Hepatic concentration of acetyl CoA varies diurnally and is highly variable across cows, depending upon lipolytic state (e.g. early postpartum period, shipping stress). Therefore, acetyl CoA is likely a key metabolite involved in both circadian control of feeding behavior and control of feed intake across physiological states. This presentation will discuss control of feed intake in animals varying in physiological state considering the effects of diet on energy partitioning and hepatic oxidation of fuels.
Keywords: feeding behavior, hepatic oxidation, metabolic fuels