CONTROL OF PROTEIN AND ENERGY-INTAKE - ROLE OF PLASMA AMINO-ACIDS AND BRAIN NEUROTRANSMITTERS

An understanding of the role that amino acids play in the regulation of normal feeding behavior is rapidly emerging. For several years it has been recognized that extremes in dietary protein content and composition cause distortion in plasma amino acid patterns and depression in food consumption of experimental animals. More recently it has become apparent that normal shifts in plasma amino acid caused by food ingestion provide signals to the brain that aid in the control of feeding behavior. The signals or relevance may arise from the function of amino acids as neurotransmitters or as precursors for neurotransmitter synthesis. At least two neuronal systems, those utilizing the neurotransmitters 5-HT and the catechols, are involved in food intake control mechanisms. These same neurotransmitters are uniquely influenced by changes in brain availability of their amino acid precursors. That is, the synthesis of 5-HT and of the catechols is directly related to availability of the precursors Trp and Tyr, respectively, in the brain. Because of the nature of brain amino acid uptake mechanisms, brain free amino acid content is acutely sensitive to that in plasma. Therefore changes in the plasma amino acid pattern may influence activity in serotonergic and catecholaminergic neurons, which in turn provides the signals required for the animal to express the appropriate response to food. Based on these relationships among diet, plasma amino acids, and brain neurotransmitter formation, the animal allowed to select among dietary options may respond by altering either quantitative or qualitative aspects of food consumption. Current evidence suggests that shifts in plasma Trp relative to other large NAA and hence in brain Trp and 5-HT provide information required for the animal to alter food preference for regulation of protein consumption. Energy, or total quantitative food intake, appears to be influenced by shifts in plasma Tyr relative to other large NAA and consequent alteration in brain Tyr and brain catecholamine activity.