Liver fatty acid composition in mice with or without nonalcoholic fatty liver disease.
Liver fatty acid composition in mice with or without nonalcoholic fatty liver disease.
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患有或不患有非酒精性脂肪肝疾病的小鼠的肝脏脂肪酸组成
DOI：
10.1186/1476-511x-10-234
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发表时间：
2011-12-14
影响因子：
4.5
通讯作者：
Zhang X
中科院分区：
文献类型：
--
作者：
Wang X;Cao Y;Fu Y;Guo G;Zhang X
背景非酒精性脂肪肝（NAFLD）是肝功能异常的最常见原因之一。由于脂肪酸会破坏生物膜，肝脏中的脂肪酸积累可能是非酒精性肝病中观察到的功能和形态学变化的部分原因。本研究的目的是使用气相色谱-质谱法来评估由高脂饲料和CCl 4诱导的实验性NAFLD小鼠模型的脂肪酸组成，并评估肝脏脂肪酸积累与NAFLD之间的关联。C57 BL/6 J小鼠连续6周给予高脂饲料以发展实验性NAFLD。同时，这些小鼠皮下注射40%CCl4-植物油混合物，每周两次。高脂饲料和CCl 4均使小鼠肝脏C14：0、C16：0、C18：0和C20：3显著升高（P < 0.01），C15：0、C18：1、C18：2和C18：3显著降低（P < 0.01）。处理还导致SFA增加和其他脂肪酸（乌法、PUFA和MUFA）减少。产物/前体n-6（C20：4/C18：2）和n-3（[C20：5+C22：6]/C18：3）的比率增加，n-6/n-3（C20：4/[C20：5+C22：6]）的比率减少，也observed.ConclusionThese数据与脂肪酸紊乱的假说一致，即高脂饲料和CCl 4诱导的非酒精性脂肪肝损伤小鼠，可能参与其发病机制和/或进展。
BackgroundNonalcoholic fatty liver disease (NAFLD) is one of the most frequent causes of abnormal liver function. Because fatty acids can damage biological membranes, fatty acid accumulation in the liver may be partially responsible for the functional and morphological changes that are observed in nonalcoholic liver disease. The aim of this study was to use gas chromatography-mass spectrometry to evaluate the fatty acid composition of an experimental mouse model of NAFLD induced by high-fat feed and CCl4and to assess the association between liver fatty acid accumulation and NAFLD. C57BL/6J mice were given high-fat feed for six consecutive weeks to develop experimental NAFLD. Meanwhile, these mice were given subcutaneous injections of a 40% CCl4-vegetable oil mixture twice per week.ResultsA pathological examination found that NAFLD had developed in the C57BL/6J mice. High-fat feed and CCl4led to significant increases in C14:0, C16:0, C18:0 and C20:3 (P < 0.01), and decreases in C15:0, C18:1, C18:2 and C18:3 (P < 0.01) in the mouse liver. The treatment also led to an increase in SFA and decreases in other fatty acids (UFA, PUFA and MUFA). An increase in the ratio of product/precursor n-6 (C20:4/C18:2) and n-3 ([C20:5+C22:6]/C18:3) and a decrease in the ratio of n-6/n-3 (C20:4/[C20:5+C22:6]) were also observed.ConclusionThese data are consistent with the hypothesis that fatty acids are deranged in mice with non-alcoholic fatty liver injury induced by high-fat feed and CCl4, which may be involved in its pathogenesis and/or progression via an unclear mechanism.