High-protein diets prevent steatosis and induce hepatic accumulation of monomethyl branched-chain fatty acids.

Autor: Garcia Caraballo SC; Department of Anatomy & Embryology, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University, Maastricht, the Netherlands., Comhair TM; Department of Anatomy & Embryology, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University, Maastricht, the Netherlands; Nutrigenomics Consortium, Top Institute of Food and Nutrition, Wageningen, the Netherlands., Houten SM; Laboratory Genetic Metabolic Diseases, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands., Dejong CH; Department of General Surgery, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University, Maastricht, the Netherlands., Lamers WH; Department of Anatomy & Embryology, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University, Maastricht, the Netherlands; Tytgat Institute for Liver and Gastrointestinal Diseases, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands; Nutrigenomics Consortium, Top Institute of Food and Nutrition, Wageningen, the Netherlands., Koehler SE; Department of Anatomy & Embryology, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University, Maastricht, the Netherlands. Electronic address: leo.koehler@maastrichtuniversity.nl.
Jazyk: angličtina
Zdroj: The Journal of nutritional biochemistry [J Nutr Biochem] 2014 Dec; Vol. 25 (12), pp. 1263-74. Date of Electronic Publication: 2014 Sep 16.
DOI: 10.1016/j.jnutbio.2014.07.005
Abstrakt: The hallmark of nonalcoholic fatty liver disease is steatosis of unknown etiology. To test how dietary protein decreases steatosis, we fed female C57BL/6 J mice low-fat (8 en%) or high-fat (42 en%) combined with low-protein (11 en%), high-protein (HP; 35 en%) or extra-high-protein (HPX; 58 en%) diets for 3 weeks. The 35 en% protein diets reduced hepatic triglyceride, free fatty acid, cholesterol and phospholipid contents to ~50% of that in 11 en% protein diets. Every additional 10 en% protein reduced hepatic fat content ~1.5 g%. HP diets had no effect on lipogenic or fatty acid-oxidizing genes except Ppargc1α (+30%), increased hepatic PCK1 content 3- to 5-fold, left plasma glucose and hepatic glycogen concentration unchanged, and decreased inflammation and cell stress (decreased Fgf21 and increased Gsta expression). The HP-mediated decrease in steatosis correlated inversely with plasma branched-chain amino-acid (BCAA) concentrations and hepatic content of BCAA-derived monomethyl branched-chain fatty acids (mmBCFAs) 14-methylpentadecanoic (14-MPDA; valine-derived) and, to a lesser extent, 14-methylhexadecanoic acid (isoleucine-derived). Liver lipid content was 1.6- to 1.8-fold higher in females than in males, but the anti-steatotic effect of HP diets was equally strong. The strong up-regulation of PCK1 and literature data showing an increase in phosphoenolpyruvate and a decline in tricarboxylic acid cycle intermediates in liver reveal that an increased efflux of these intermediates from mitochondria represents an important effect of an HP diet. The HP diet-induced increase in 14-MPDA and the dietary response in gene expression were more pronounced in females than males. Our findings are compatible with a facilitating role of valine-derived mmBCFAs in the antisteatotic effect of HP diets.
(Copyright © 2014 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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