The control of energy intake is complex, including mechanisms that act independently (e.g. distention, osmotic effects, fuel-sensing) as well as interacting factors that are likely to affect feeding via their effects on hepatic oxidation. Effects of ruminant diets on feed intake vary greatly because of variation in their filling effects, as well as the type and temporal absorption of fuels. Effects of nutrients on endocrine response and gene expression affect energy partitioning, which in turn affects feeding behaviour by altering clearance of fuels from the blood. Dominant mechanisms controlling feed intake change with physiological state, which is highly variable among ruminants, especially through the lactation cycle. Ruminal distention might dominate control of feed intake when ruminants consume low-energy diets or when energy requirements are high, but fuel-sensing by tissues is likely to dominate control of feed intake when fuel supply is in excess of that required. The liver is likely to be a primary sensor of energy status because it is supplied by fuels from the portal drained viscera as well as the general circulation, it metabolises a variety of fuels derived from both the diet and tissues, and a signal related to hepatic oxidation of fuels is conveyed to feeding centres in the brain by hepatic vagal afferents stimulating or inhibiting feeding, depending on its energy status. The effects of somatotropin on export of fuels by milk secretion, effects of insulin on gluconeogenesis, and both on mobilisation and repletion of tissues, determine fuel availability and feed intake over the lactation cycle. Control of feed intake by hepatic energy status, affected by oxidation of fuels, is an appealing conceptual model because it integrates effects of various fuels and physiological states on feeding behaviour.
Effects of propionate and carnitine on the hepatic oxidation of short- and medium-chain-length fatty acids
