Nonalcoholic Fatty Liver Disease and Omega-3 Fatty Acids: Mechanisms and Clinical Use

被引：27

作者：

Spooner, Melinda H. ^{[1
]}

Jump, Donald B. ^{[1
]}

机构：

[1] Oregon State Univ, Sch Biol & Populat Hlth Sci, Mol Nutr & Diabet Res Lab, Corvallis, OR 97331 USA

来源：

ANNUAL REVIEW OF NUTRITION | 2023年 / 43卷

基金：

美国国家卫生研究院;

关键词：

docosahexaenoic acid; nonalcoholic steatohepatitis; steatosis; inflammation; fibrosis; OXIDATIVE STRESS; INSULIN-RESISTANCE; HEPATIC STEATOSIS; ACID-COMPOSITION; GENE-EXPRESSION; LINOLEIC-ACID; BILE-ACIDS; RECEPTOR; FIBROSIS; IMPACT;

D O I：

10.1146/annurev-nutr-061021-030223

中图分类号：

R15 [营养卫生、食品卫生]; TS201 [基础科学];

学科分类号：

100403 ;

摘要：

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic fatty liver disease worldwide, particularly in obese and type 2 diabetic individuals. Currently, there are no therapies for NAFLD that have been approved by the US Food and Drug Administration. Herein, we examine the rationale for using omega 3 polyunsaturated fatty acids (PUFAs) in NAFLD therapy. This focus is based on the finding that NAFLD severity is associated with a reduction of hepatic C20-22 omega 3 PUFAs. Because C20-22 omega 3 PUFAs are pleiotropic regulators of cell function, loss of C20-22 omega 3 PUFAs has the potential to significantly impact hepatic function. We describe NAFLD prevalence and pathophysiology as well as current NAFLD therapies. We also present evidence from clinical and preclinical studies that evaluated the capacity of C20-22 omega 3 PUFAs to treat NAFLD. Given the clinical and preclinical evidence, dietary C20-22 omega 3 PUFA supplementation has the potential to decrease human NAFLD severity by reducing hepatosteatosis and liver injury.

引用

页码：199 / 223

页数：25

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