[多不饱和脂肪酸抑制非酒精性脂肪肝发病和恶化的分子机制]。

IF 0.3 4区 医学 Q4 PHARMACOLOGY & PHARMACY
Misa Ando, Hyeon-Cheol Lee-Okada, Takehiko Yokomizo
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本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Molecular Mechanisms by Which Polyunsaturated Fatty Acids Suppress the Pathogenesis and Progression of NAFLD].

In recent years, the number of people suffering from lifestyle diseases such as hyperlipidemia and fatty liver disease has increased rapidly due to westernization of dietary patterns. Among fatty liver diseases, those that are not caused by alcohol are referred to as nonalcoholic fatty liver disease (NAFLD). Some NAFLD can progress to nonalcoholic steatohepatitis (NASH), and further progression of NAFLD can lead to cirrhosis and liver cancer. Although numerous studies have demonstrated the efficacy of dietary polyunsaturated fatty acids (PUFAs), particularly omega-3 PUFAs eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), against NAFLD, the detailed mechanisms by which these PUFAs exert their protective effects on the pathogenesis and progression of NAFLD are not well understood. Recent studies using knockout mouse models and genome-wide association studies have suggested a potential role for the enzymes responsible for the biosynthesis of PUFAs (FADS1, FADS2, ELOVL2, and ELOVL5) and their incorporation into phospholipids (LPCAT3/MBOAT5/LPLAT12 and LPIAT1/MBOAT7/LPLAT11) in the development of NAFLD. In this review, we summarize recent findings on the association of NAFLD and PUFAs with a focus on PUFA biosynthetic and metabolic enzymes to discuss the potential role of PUFAs in the prevention of NAFLD.

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来源期刊
CiteScore
0.60
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发文量
169
审稿时长
1 months
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