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首页> 外文期刊>The Journal of Nutritional Biochemistry >High-protein diets prevent steatosis and induce hepatic accumulation of monomethyl branched-chain fatty acids
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High-protein diets prevent steatosis and induce hepatic accumulation of monomethyl branched-chain fatty acids

机译：高蛋白饮食可预防脂肪变性并诱导肝内单甲基支链脂肪酸的蓄积

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摘要

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 similar to 50% of that in 11 en% protein diets. Every additional 10 en% protein reduced hepatic fat content similar to 1.5 g%. HP diets had no effect on lipogenic or fatty acid-oxidizing genes except Ppargc1 alpha (+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 antisteatotic 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. (C) 2014 Elsevier Inc. All rights reserved.
机译：非酒精性脂肪肝的标志是病因不明的脂肪变性。为了测试饮食蛋白如何减少脂肪变性，我们给雌性C57BL / 6 J小鼠低脂（8 en％）或高脂（42 en％）结合低蛋白（11 en％），高蛋白（HP; 35周）或超高蛋白饮食（HPX; 58周），持续3周。 35％的蛋白质饮食减少了肝甘油三酸酯，游离脂肪酸，胆固醇和磷脂的含量，与11％的蛋白质饮食减少了50％的相似。每增加10 en％的蛋白质，肝脂肪含量减少约1.5 g％。除Ppargc1 alpha（+ 30％），肝PCK1含量增加3至5倍，血浆葡萄糖和肝糖原浓度不变，发炎和细胞应激降低（减少）外，HP饮食对脂肪形成或脂肪酸氧化基因无影响Fgf21和Gsta表达增加）。 HP介导的脂肪变性减少与血浆支链氨基酸（BCAA）浓度和BCAA衍生的单甲基支链脂肪酸（mmBCFA）14-甲基十五烷酸（14-MPDA;缬氨酸衍生）的肝脏含量成反比，在较小程度上是14-甲基十六烷酸（异亮氨酸衍生）。女性的肝脏脂质含量比男性高1.6到1.8倍，但HP饮食的抗脂肪变性作用同样很强。 PCK1的强烈上调和文献数据显示，磷酸烯醇丙酮酸的增加和肝脏中三羧酸循环中间体的减少表明，线粒体这些中间体的外排增加代表了HP饮食的重要作用。 HP饮食引起的14-MPDA的增加和饮食对基因表达的反应在女性中比男性更为明显。我们的发现与缬氨酸衍生的mmBCFA在HP饮食的抗脂肪变性作用中的促进作用相吻合。 （C）2014 Elsevier Inc.保留所有权利。

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