Dietary protein insufficiency: an important consideration in fatty liver disease?
Dietary protein insufficiency: an important consideration in fatty liver disease?
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DOI：
10.1017/s0007114519003064
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发表时间：
2020-03-28
影响因子：
3.6
通讯作者：
Griffiths, Helen R.
中科院分区：
文献类型：
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作者：
Ampong, Isaac;Watkins, Adam;Griffiths, Helen R.
在发展中国家，膳食蛋白质不足与TAG过量储存和非酒精性脂肪肝（NAFLD）有关。低蛋白饮食后肝脏TAG蓄积可能是由于过氧化物酶体、线粒体和肠道微生物群功能改变所致。肝脏过氧化物酶体和线粒体通常介导营养物质的代谢，为脂肪生成提供能量和底物。过氧化物酶体的生物合成和活性可以通过来自肠道细菌的奇链脂肪酸（OCFA）和SCFA（例如丙酸盐和丁酸盐）来调节。在过氧化物酶体和线粒体的氨基酸代谢过程中也产生丙酸和丁酸浓度，与肥胖、胰岛素抵抗和NAFLD的风险呈负相关。在这篇水平扫描综述中，我们收集了关于蛋白质营养不良对OCFA产生影响的现有证据，这些证据来自线粒体，过氧化物酶体和肠道微生物群功能的丧失，以及其与肝脏中脂质积累的相关性。膳食蛋白质的甲基供体氨基酸组成是肝功能和脂质储存的重要贡献者;膳食支链氨基酸的存在和丰度可以调节肠道微生物组的组成和代谢活性，另一方面，可以影响肝脏中保护性OCFA和SCFA的产生。在饲喂低蛋白饮食的临床前动物模型中，补充特定的氨基酸可以改善脂肪肝疾病。膳食蛋白质摄入量低与脂肪肝之间的关系尚未得到充分研究，值得进一步调查，特别是在发展中国家膳食蛋白质限制的弱势群体中。
Dietary protein insufficiency has been linked to excessive TAG storage and non-alcoholic fatty liver disease (NAFLD) in developing countries. Hepatic TAG accumulation following a low-protein diet may be due to altered peroxisomal, mitochondrial and gut microbiota function. Hepatic peroxisomes and mitochondria normally mediate metabolism of nutrients to provide energy and substrates for lipogenesis. Peroxisome biogenesis and activities can be modulated by odd-chain fatty acids (OCFA) and SCFA that are derived from gut bacteria, for example, propionate and butyrate. Also produced during amino acid metabolism by peroxisomes and mitochondria, propionate and butyrate concentrations correlate inversely with risk of obesity, insulin resistance and NAFLD. In this horizon-scanning review, we have compiled available evidence on the effects of protein malnutrition on OCFA production, arising from loss in mitochondrial, peroxisomal and gut microbiota function, and its association with lipid accumulation in the liver. The methyl donor amino acid composition of dietary protein is an important contributor to liver function and lipid storage; the presence and abundance of dietary branched-chain amino acids can modulate the composition and metabolic activity of the gut microbiome and, on the other hand, can affect protective OCFA and SCFA production in the liver. In preclinical animal models fed with low-protein diets, specific amino acid supplementation can ameliorate fatty liver disease. The association between low dietary protein intake and fatty liver disease is underexplored and merits further investigation, particularly in vulnerable groups with dietary protein restriction in developing countries.