Protein, amino acids and the control of food intakePotier, Mylènea; Darcel, Nicolasa,b; Tomé, Daniela,bCurrent Opinion in Clinical Nutrition and Metabolic Care: January 2009 - Volume 12 - Issue 1 - p 54–58 doi: 10.1097/MCO.0b013e32831b9e01 Protein, amino acid metabolism and therapy: Edited by Erich Roth and Elena Volpi Buy Abstract Author InformationAuthors Article MetricsMetrics Purpose of review The present review presents recent findings on peripheral and central pathways involved in protein and amino acid-induced satiety. Recent findings A high-protein load leads to a higher decrease of energy intake at the next meal than carbohydrate and fat. A protein-enriched diet induces satiety, improves body composition and results in weight loss. At the peripheral level, proteins seem to induce the release of anorexigenic gut hormones cholecystokinin, glucagon-like peptide-1 and peptide YY, whereas the involvement of ghrelin remains uncertain. Energy expenditure and glucose are probably involved as metabolic signals in protein-induced satiety. Moreover, there is some evidence that the circulating level of leucine could impact food intake. Leucine has been shown to modulate the activity of the energy and nutrient sensor pathways controlled by AMPK and mTOR in the hypothalamus. Moreover, high-protein diets lead to activation of the noradrenergic/adrenergic neuronal pathway in the nucleus of the solitary tract and in melanocortin neurons in the arcuate nucleus. Summary Complex and redundant pathways are involved in protein and amino acid-induced satiety. Significant advances have recently allowed a better understanding of the involved cellular and molecular mechanisms. The involvement of some specific area of the brain including the hypothalamus and the nucleus of the solitary tract has to be further analyzed. aINRA, France bAgroParisTech, CNRH-IdF, UMR914 Nutrition Physiology and Ingestive Behavior, Paris, France Correspondence to Daniel Tomé, UMR 914 INRA/AgroParisTech, 16 rue Claude Bernard, 75231 Paris Cedex 05, France Tel: +33 1 44 08 17 18; e-mail: email@example.com © 2009 Lippincott Williams & Wilkins, Inc.