Amino Acid Signals and Food Intake and Preference: Relation to Body Protein Metabolism

Publisher Website
Google Scholar
Abstract
Depressed food consumption is an early response of experimental, animals to: 1) a dietary deficiency of either protein or an individual indispensable amino acid; 2) a distortion of the dietary pattern of amino acids when protein intake is low; and 3) a substantial elevation in the protein content of the diet. In each of these conditions the change in feeding behaviour is associated with alterations in concentrations of amino acids in blood but in none of them has the biochemical basis for the depressed food intake been established. The depressed food intake of rats consuming a low protein diet in which an imbalance of amino acids has been created by adding quantities of amino acids other than the one most limiting for growth, is associated with elevations in the plasma concentrations of amino acids added to create the imbalance and usually with a depression in the plasma concentration of the growth-limiting amino acid. These changes, in turn, are associated with depression of the concentration of the growth-limiting amino acid in the brain free amino acid pool. Studies in which uptake of amino acids into brain slices has been examined support the conclusion that various distortions of the plasma amino acid pattern, as the result of dietary imbalances of amino acids, can lead to depletion of the brain pool of a specific amino acid through competition between it and other amino acids in surplus in plasma for uptake into brain. The results of studies with rats in vivo of the effects on brain amino acid pools of ingestion of diets containing supplements of amino acids that compete with the growth-limiting amino acid for uptake into brain also support this conclusion. Depletion of the brain pool of the limiting amino acid as the result of feeding a diet with an amino acid imbalance can be related to overall body protein metabolism. In the young growing animal, protein synthesis is stimulated after a meal. Thus, when the diet is limiting in a single amino acid, that amino acid will be depleted from the circulating body pool. At the same time, the activities of amino acid degrading enzymes are low in animals fed a low protein diet; hence, such animals have limited capacity to degrade surpluses of amino acids. These conditions, depletion of the blood pool of the limiting amino acid and slow removal of surpluses of competing amino acids from the blood, will increase the extent of competition between other amino acids and the limiting amino acid for uptake into brain. The relationship between depletion of the brain pool of the limiting amino acid and the signal for depressed food intake under these conditions has not been established. The depressed food intake of rats fed a high protein diet is associated with substantial elevations of blood amino acid concentrations, particularly of the large neutral amino acids. As elevations in the concentrations of large neutral amino acids in blood can suppress uptake of tryptophan into brain, it has been postulated that protein consumption may be responsive to changes in brain tryptophan concentration and that this response may be mediated by changes in brain concentration of serotonin, a neurotransmitter formed from tryptophan. Studies of associations among protein consumption and brain tryptophan and serotonin concentrations both in rats fed single diets differing in protein content and in rats offered a choice between two diets differing in protein content, have not supported this hypothesis. Measurements of brain amino acid concentrations of rats at various times during and after adaptation to a high protein intake suggest that brain total free amino acid concentration may play a role in the control of protein intake and, hence, of food intake. The degree of food intake depression observed in rats fed diets differing in protein content appears to depend on the capacity of the body to degrade amino acids. When food intake is depressed initially in response to increased dietary protein content, brain total indispensable amino acid concentration is about 2.5 mM. In rats that have been fed previously a diet that is low in protein, and therefore have a limited ability to degrade amino acids, this concentration of brain amino acids is associated with depressed food intake. If rats are allowed to become adapted to a high protein intake, their capacity for amino acid degradation (activities of amino acid-degrading enzymes) increases substantially. After adaptation, they can consume much larger quantities of protein before brain indispensable amino acid concentrations reach 2.5 mM. Also, rats that have been adapted to low protein diets and are then fed a high protein meal tend to reject high protein diets when they are subsequently offered a choice between low and high protein diets. Rats that have been adapted to high protein diets, and have the capacity to clear amino acids rapidly from blood, select diets higher in protein content under these conditions. The correlation between protein consumption and brain amino acid concentrations is such as to suggest that total body amino acid-degrading capacity determines the extent to which brain amino acid concentrations rise in response to changes in dietary protein intake and that the extent of this rise may be a factor in the control of subsequent protein consumption.