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首页> 外文期刊>Alcohol >Role of fatty liver, dietary fatty acid supplements, and obesity in the progression of alcoholic liver disease: introduction and summary of the symposium.
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Role of fatty liver, dietary fatty acid supplements, and obesity in the progression of alcoholic liver disease: introduction and summary of the symposium.

机译：脂肪肝，膳食脂肪酸补充剂和肥胖在酒精性肝病进展中的作用：研讨会的引入和概述。

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Alcoholic liver disease is a major cause of illness and death in the United States. In the initial stages of the disease, fat accumulation in hepatocytes leads to the development of fatty liver (steatosis), which is a reversible condition. If alcohol consumption is continued, steatosis may progress to hepatitis and fibrosis, which may lead to liver cirrhosis. Alcoholic fatty liver has long been considered benign; however, increasing evidence supports the idea that it is a pathologic condition. Blunting of the accumulation of fat within the liver during alcohol consumption may block or delay the progression of fatty liver to hepatitis and fibrosis. To achieve this goal, it is important to understand the underlying biochemical and molecular mechanisms by which chronic alcohol consumption leads to fat accumulation in the liver and fatty liver progresses to hepatitis and fibrosis. In addition to alcohol consumption, dietary fatty acids and obesity have been shown to affect the degree of fat accumulation within the liver. Again, it is important to know how these factors modulate the progression of alcoholic liver disease. The National Institute on Alcohol Abuse and Alcoholism and the Office of Dietary Supplements, National Institutes of Health, sponsored a symposium on "Role of Fatty Liver, Dietary Fatty Acid Supplements, and Obesity in the Progression of Alcoholic Liver Disease" in Bethesda, Maryland, USA, October 2003. The following is a summary of the symposium. Alcoholic fatty liver is a pathologic condition that may predispose the liver to further injury (hepatitis and fibrosis) by cytochrome P450 2E1 induction, free radical generation, lipid peroxidation, nuclear factor-kappa B activation, and increased transcription of proinflammatory mediators, including tumor necrosis factor-alpha. Increased acetaldehyde production and lipopolysaccharide-induced Kupffer cell activation may further exacerbate liver injury. Acetaldehyde may promote hepatic fat accumulation by impairing the ability of peroxisome proliferator-activated receptor alpha to bind DNA, and by increasing the synthesis of sterol regulatory binding protein-1. Unsaturated fatty acids (corn oil, fish oil) exacerbate alcoholic liver injury by accentuating oxidative stress, whereas saturated fatty acids are protective. Polyenylphosphatidylcholine may prevent liver injury by down-regulating cytochrome P450 2E1 activity, attenuating oxidative stress, reducing the number of activated hepatic stellate cells, and up-regulating collagenase activity. Nonalcoholic steatohepatitis may develop through several mechanisms, such as oxidative stress, mitochondrial dysfunction and associated impaired fat metabolism, dysregulated cytokine metabolism, insulin resistance, and altered methionine/S-adenosylmethionine/homocysteine metabolism. Obesity (adipose tissue) may contribute to the development of alcoholic liver disease by generating free radicals, increasing tumor necrosis factor-alpha production, inducing insulin resistance, and producing fibrogenic agents, such as angiotensin II, norepinephrine, neuropeptide Y, and leptin. Finally, alcoholic fatty liver transplant failure may be linked to oxidative stress. In vitro treatment of fatty livers with interleukin-6 may render allografts safer for clinical transplantation.
机译：酒精性肝病是美国疾病和死亡的主要原因。在疾病的初始阶段，肝细胞的脂肪积累导致脂肪肝（脂肪变性）的发育，这是一种可逆条件。如果继续饮酒，脂肪变性可能会导致肝炎和纤维化可能导致肝硬化。酒精脂肪肝长期以来一直被认为是良性的;然而，越来越多的证据支持这是一种病理状况。在饮酒期间肝脏脂肪积聚的脂肪可能会阻断或延迟脂肪肝的进展到肝炎和纤维化。为了实现这一目标，重要的是要了解慢性酒精消耗导致肝脏和脂肪肝中脂肪积聚的潜在生化和分子机制进展到肝炎和纤维化。除酒精消耗外，还已显示膳食脂肪酸和肥胖症来影响肝脏内的脂肪积累程度。同样，重要的是要知道这些因素如何调节酒精性肝病的进展。国家酒精滥用和酗酒研究所和膳食补充剂办公室，国家卫生研究院，赞助了“脂肪肝，饮食脂肪酸补充剂和肥胖在酒精性肝病进展中的作用”的研讨会，马里兰州美国，2003年10月。以下是研讨会的摘要。酒精脂肪肝是一种病理条件，可以使肝脏进一步损伤（肝炎和纤维化）通过细胞色素P450 2E1诱导，自由基产生，脂质过氧化，核因子-κB激活，以及增加促炎介质的转录，包括肿瘤坏死因子α。增加的乙醛生产和脂多糖诱导的Kupffer细胞活化可能进一步加剧肝损伤。乙醛可以通过损害过氧化物激素激活的受体α结合DNA的能力来促进肝脂肪积累，并通过增加甾醇调节结合蛋白-1的合成。不饱和脂肪酸（玉米油，鱼油）通过诱发氧化应激加剧酒精性肝损伤，而饱和脂肪酸是保护性的。聚苯基磷脂酰胆碱可以通过下调细胞色素P450 2E1活性，衰减氧化应激，减少活化的肝星状细胞的数量，降低升压胶原酶活性的肝损伤。非酒精脂肪型肝炎可能通过若干机制而发展，例如氧化应激，线粒体功能障碍和相关的脂肪代谢，具有多疑细胞因子代谢，胰岛素抵抗和改变的甲硫氨酸/ S-腺苷甲基甲基甲基/同态代谢。肥胖症（脂肪组织）可以通过产生自由基，增加肿瘤坏死因子-α产生，诱导胰岛素抗性和产生纤维原子，如血管紧张素II，去甲肾上腺素，神经肽Y和瘦蛋白来促进酒精性肝病的发展。最后，酒精性脂肪肝移植失败可能与氧化应激相关。用白细胞介素-6对脂肪肝的体外处理可以使同种异体移植物更安全地进行临床移植。

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