Nassir Fatiha, Rector R Scott, Hammoud Ghassan M, Ibdah Jamal A
Dr Nassir is an assistant research professor of medicine in the Division of Gastroenterology and Hepatology at the University of Missouri School of Medicine in Columbia, Missouri. Dr Rector is an assistant professor of medicine in the Division of Gastroenterology and Hepatology and the Department of Nutrition and Exercise Physiology at the University of Missouri School of Medicine; he is also a research health scientist in the Research Service at the Harry S. Truman Memorial Veterans' Hospital in Columbia, Missouri. Dr Hammoud is an associate professor of clinical medicine in the Division of Gastroenterology and Hepatol ogy at the University of Missouri School of Medicine. Dr Ibdah is a professor of medicine in the Division of Gastroenterology and Hepatology and the Department of Nutrition and Exercise Physiology at the University of Missouri School of Medicine, where he is also the director of the Division of Gastroenterology and Hepatology; in addition, he is a research health scientist in the Research Service at the Harry S. Truman Memorial Veterans' Hospital.
Gastroenterol Hepatol (N Y). 2015 Mar;11(3):167-75.
Hepatic steatosis is defined as intrahepatic fat of at least 5% of liver weight. Simple accumulation of triacylglycerols in the liver could be hepatoprotective; however, prolonged hepatic lipid storage may lead to liver metabolic dysfunction, inflammation, and advanced forms of nonalcoholic fatty liver disease. Nonalcoholic hepatic steatosis is associated with obesity, type 2 diabetes, and dyslipidemia. Several mechanisms are involved in the accumulation of intrahepatic fat, including increased flux of fatty acids to the liver, increased de novo lipogenesis, and/or reduced clearance through β-oxidation or very-low-density lipoprotein secretion. This article summarizes the mechanisms involved in the accumulation of triacylglycerols in the liver, the clinical implications, and the prevention of hepatic steatosis, with a focus on the role of mitochondrial function and lifestyle modifications.
肝脂肪变性被定义为肝脏内脂肪含量至少占肝脏重量的5%。肝脏中三酰甘油的单纯蓄积可能具有肝脏保护作用;然而,肝脏脂质的长期储存可能导致肝脏代谢功能障碍、炎症以及非酒精性脂肪性肝病的晚期形式。非酒精性肝脂肪变性与肥胖、2型糖尿病和血脂异常有关。肝内脂肪蓄积涉及多种机制,包括脂肪酸向肝脏的流量增加、从头脂肪生成增加和/或通过β氧化或极低密度脂蛋白分泌的清除减少。本文总结了肝脏中三酰甘油蓄积所涉及的机制、临床意义以及肝脂肪变性的预防,重点关注线粒体功能和生活方式改变的作用。