Increase in long-chain polyunsaturated fatty acid n-6/n-3 ratio in relation to hepatic steatiosis in patients with non-alcoholic fatty liver disease
Increase in long-chain polyunsaturated fatty acid n-6/n-3 ratio in relation to hepatic steatiosis in patients with non-alcoholic fatty liver disease
复制标题
DOI：
10.1042/cs20030326
复制
发表时间：
2004-06-01
期刊：
影响因子：
6
通讯作者：
Poniachik, J
中科院分区：
文献类型：
--
作者：
Araya, J;Rodrigo, R;Poniachik, J
肝脂肪变性是与NAFLD（非酒精性脂肪性肝病）相关的一个主要特征。本研究的目的是评估NAFLD患者肝脏总脂、甘油三酯和磷脂中PUFA（多不饱和脂肪酸）水平与脂肪组织中PUFA水平的关系，以及与氧化应激相关的肝脏指标作为肝脂肪变性的因素。研究对象为11例对照和19例NAFLD患者。肝脏和腹部脂肪组织脂肪酸采用GLC法进行分析。以肝脏蛋白质羰基含量和丙二醛含量作为氧化应激的相关指标。NAFLD患者肝脏三酰基甘油中n - 6和n - 3系列的LCPUFA（长链PUFA）减少，20:4,n - 6/18:2，n - 6和(20:5,n - 3 + 22:6,n - 3)/18:3，n - 3比例降低，而肝脏磷脂含有较高的n - 6和较低的n - 3 LCPUFA。这些发现伴随着(i)肝脏和脂肪组织中n - 6/n - 3比值的增加，（ii）脂肪组织中n - 9反式水平18:1的增加，以及（iii）肝脏脂质过氧化和蛋白质氧化指数的增加。由此得出结论，NAFLD患者肝脏中LCPUFA n - 6/n - 3比值显著增强，这种情况可能有利于脂质合成而不是氧化和分泌，从而导致脂肪变性。肝脏LCPUFA的消耗可能是由于PUFA去饱和缺陷，由于前体摄入不足，如18:3，n - 3，以及18:1，n - 9反式异构体摄入过多导致去饱和酶抑制，以及由于氧化应激导致LCPUFA过氧化增加。
Hepatic steatosis is a major feature associated with NAFLD (non-alcoholic fatty liver disease). The aims of the present study were to assess the levels of PUFA (polyunsaturated fatty acids) in liver total lipids, triacylglycerols (triglycerides) and phospholipids of NAFLD patients in relation to those in adipose tissue and hepatic indexes related to oxidative stress as factors contributing to hepatic steatosis. Eleven control subjects and 19 patients with NAFLD were studied. Analysis of liver and abdominal adipose tissue fatty acids was carried out by GLC. The liver content of protein carbonyl groups and malondialdehyde were taken as indexes related to oxidative stress. NAFLD patients had a depletion in LCPUFA (long-chain PUFA) of the n - 6 and n - 3 series in liver triacylglycerols, with decreased 20:4,n - 6/18:2,n - 6 and (20:5,n - 3 + 22:6,n - 3)/18:3,n - 3 ratios, whereas liver phospholipids contained higher n - 6 and lower n - 3 LCPUFA. These findings were accompanied by an enhancement of (i) n - 6/n - 3 ratio in liver and adipose tissue, (ii) 18:1,n - 9 trans levels in adipose tissue, and (iii) hepatic lipid peroxidation and protein oxidation indexes. It is concluded that a marked enhancement in LCPUFA n - 6/n - 3 ratio occurs in the liver of NAFLD patients, a condition that may favour lipid synthesis over oxidation and secretion, thereby leading to steatosis. Depletion of hepatic LCPUFA may result from both defective desaturation of PUFA, due to inadequate intake of precursors, such as 18:3,n - 3, and higher intake of the 18:1,n - 9 trans isomer leading to desaturase inhibition, and from an increased peroxidation of LCPUFA due to oxidative stress.