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1
Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity.肝内脂肪而非内脏脂肪与肥胖的代谢并发症相关。
Proc Natl Acad Sci U S A. 2009 Sep 8;106(36):15430-5. doi: 10.1073/pnas.0904944106. Epub 2009 Aug 24.
2
Relationship between body fat mass and free fatty acid kinetics in men and women.男性和女性体脂肪量与游离脂肪酸动力学之间的关系。
Obesity (Silver Spring). 2009 Oct;17(10):1872-7. doi: 10.1038/oby.2009.224. Epub 2009 Jul 23.
3
Liver fat and lipid oxidation in humans.人体中的肝脏脂肪与脂质氧化
Liver Int. 2009 Oct;29(9):1439-46. doi: 10.1111/j.1478-3231.2009.02076.x. Epub 2009 Jul 7.
4
Dietary fat and carbohydrates differentially alter insulin sensitivity during caloric restriction.在热量限制期间,膳食脂肪和碳水化合物对胰岛素敏感性的影响有所不同。
Gastroenterology. 2009 May;136(5):1552-60. doi: 10.1053/j.gastro.2009.01.048. Epub 2009 Jan 25.
5
Endoplasmic reticulum stress is reduced in tissues of obese subjects after weight loss.体重减轻后,肥胖受试者组织中的内质网应激反应有所减轻。
Diabetes. 2009 Mar;58(3):693-700. doi: 10.2337/db08-1220. Epub 2008 Dec 9.
6
Analysis of hepatic genes involved in the metabolism of fatty acids and iron in nonalcoholic fatty liver disease.非酒精性脂肪性肝病中脂肪酸和铁代谢相关肝基因分析。
Hepatol Res. 2009 Apr;39(4):366-73. doi: 10.1111/j.1872-034X.2008.00464.x. Epub 2008 Nov 25.
7
Storing up trouble: does accumulation of intramyocellular triglyceride protect skeletal muscle from insulin resistance?埋下隐患:肌内甘油三酯的积累能否保护骨骼肌免受胰岛素抵抗?
Clin Exp Pharmacol Physiol. 2009 Jan;36(1):5-11. doi: 10.1111/j.1440-1681.2008.05075.x. Epub 2008 Oct 15.
8
Increased expression and activity of hepatic lipase in the liver of morbidly obese adult patients in relation to lipid content.肥胖症成年患者肝脏中肝脂酶的表达和活性增加与脂质含量有关。
Obes Surg. 2009 Jul;19(7):894-904. doi: 10.1007/s11695-008-9739-9. Epub 2008 Oct 30.
9
Recent insights into hepatic lipid metabolism in non-alcoholic fatty liver disease (NAFLD).非酒精性脂肪性肝病(NAFLD)中肝脏脂质代谢的最新见解。
Prog Lipid Res. 2009 Jan;48(1):1-26. doi: 10.1016/j.plipres.2008.08.001. Epub 2008 Sep 9.
10
Genetic variation in PNPLA3 confers susceptibility to nonalcoholic fatty liver disease.PNPLA3基因变异会使人易患非酒精性脂肪性肝病。
Nat Genet. 2008 Dec;40(12):1461-5. doi: 10.1038/ng.257. Epub 2008 Sep 25.

肥胖与非酒精性脂肪性肝病:生化、代谢及临床意义。

Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications.

机构信息

Center for Human Nutrition and Atkins Center of Excellence in Obesity Medicine, Washington University School of Medicine, St Louis, MO 63110-1093, USA.

出版信息

Hepatology. 2010 Feb;51(2):679-89. doi: 10.1002/hep.23280.

DOI:10.1002/hep.23280
PMID:20041406
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3575093/
Abstract

Obesity is associated with an increased risk of nonalcoholic fatty liver disease (NAFLD). Steatosis, the hallmark feature of NAFLD, occurs when the rate of hepatic fatty acid uptake from plasma and de novo fatty acid synthesis is greater than the rate of fatty acid oxidation and export (as triglyceride within very low-density lipoprotein). Therefore, an excessive amount of intrahepatic triglyceride (IHTG) represents an imbalance between complex interactions of metabolic events. The presence of steatosis is associated with a constellation of adverse alterations in glucose, fatty acid, and lipoprotein metabolism. It is likely that abnormalities in fatty acid metabolism, in conjunction with adipose tissue, hepatic, and systemic inflammation, are key factors involved in the development of insulin resistance, dyslipidemia, and other cardiometabolic risk factors associated with NAFLD. However, it is not clear whether NAFLD causes metabolic dysfunction or whether metabolic dysfunction is responsible for IHTG accumulation, or possibly both. Understanding the precise factors involved in the pathogenesis and pathophysiology of NAFLD will provide important insights into the mechanisms responsible for the cardiometabolic complications of obesity.

摘要

肥胖与非酒精性脂肪性肝病(NAFLD)的风险增加有关。当肝脏从血浆中摄取脂肪酸和从头合成脂肪酸的速度大于脂肪酸氧化和输出(作为极低密度脂蛋白中的甘油三酯)的速度时,就会发生 NAFLD 的标志性特征——脂肪变性。因此,肝内甘油三酯(IHTG)过多代表代谢事件复杂相互作用之间的失衡。脂肪变性的存在与葡萄糖、脂肪酸和脂蛋白代谢的一系列不良改变有关。脂肪代谢异常与脂肪组织、肝和全身炎症一起,很可能是与 NAFLD 相关的胰岛素抵抗、血脂异常和其他心血管代谢危险因素发展的关键因素。然而,尚不清楚是 NAFLD 导致代谢功能障碍,还是代谢功能障碍导致 IHTG 积聚,或者可能两者兼而有之。了解 NAFLD 的发病机制和病理生理学中涉及的确切因素,将为肥胖相关的心血管代谢并发症的机制提供重要的见解。