Homeostatic sensing of dietary protein restriction: A case for FGF21
- PMID: 29890191
- PMCID: PMC6175661
- DOI: 10.1016/j.yfrne.2018.06.002
Homeostatic sensing of dietary protein restriction: A case for FGF21
Abstract
Restriction of dietary protein intake increases food intake and energy expenditure, reduces growth, and alters amino acid, lipid, and glucose metabolism. While these responses suggest that animals 'sense' variations in amino acid consumption, the basic physiological mechanism mediating the adaptive response to protein restriction has been largely undescribed. In this review we make the case that the liver-derived metabolic hormone FGF21 is the key signal which communicates and coordinates the homeostatic response to dietary protein restriction. Support for this model centers on the evidence that FGF21 is induced by the restriction of dietary protein or amino acid intake and is required for adaptive changes in metabolism and behavior. FGF21 occupies a unique endocrine niche, being induced when energy intake is adequate but protein and carbohydrate are imbalanced. Collectively, the evidence thus suggests that FGF21 is the first known endocrine signal of dietary protein restriction.
Keywords: Dietary protein; FGF21; Macronutrient; Nutrition.
Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.
References
-
- Anderson SA, Tews JK & Harper AE, 1990. Dietary branched-chain amino acids and protein selection by rats. J Nutr. 120, 52–63. - PubMed
-
- Angelin B, Larsson TE & Rudling M, 2012. Circulating fibroblast growth factors as metabolic regulators-a critical appraisal. Cell Metab. 16, 693–705. - PubMed
-
- Anthony TG & Gietzen DW, 2013. Detection of amino acid deprivation in the central nervous system. Curr Opin Clin Nutr Metab Care. 16, 96–101. - PubMed
-
- Anthony TG, McDaniel BJ, Byerley RL, McGrath BC, Cavener DR, McNurlan MA & Wek RC, 2004. Preservation of liver protein synthesis during dietary leucine deprivation occurs at the expense of skeletal muscle mass in mice deleted for eIF2 kinase GCN2. J Biol Chem. 279, 36553–36561. - PubMed
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