Vyas Diwakar, Kadegowda Anil Kumar G, Erdman Richard A
Department of Animal and Avian Sciences, University of Maryland, College Park, MD 20742, USA.
J Nutr Metab. 2012;2012:932928. doi: 10.1155/2012/932928. Epub 2011 Aug 22.
Objective. To summarize the recent studies on effect of conjugated linoleic acid (CLA) on hepatic steatosis and hepatic and adipose lipid metabolism highlighting the potential regulatory mechanisms. Methods. Sixty-four published experiments were summarized in which trans-10, cis-12 CLA was fed either alone or in combination with other CLA isomers to mice, rats, hamsters, and humans were compared. Summary and Conclusions. Dietary trans-10, cis-12 CLA induces a severe hepatic steatosis in mice with a more muted response in other species. Regardless of species, when hepatic steatosis was present, a concurrent decrease in body adiposity was observed, suggesting that hepatic lipid accumulation is a result of uptake of mobilized fatty acids (FA) from adipose tissue and the liver's inability to sufficiently increase FA oxidation and export of synthesized triglycerides. The potential role of liver FA composition, insulin secretion and sensitivity, adipokine, and inflammatory responses are discussed as potential mechanisms behind CLA-induced hepatic steatosis.
目的。总结共轭亚油酸（CLA）对肝脂肪变性以及肝脏和脂肪组织脂质代谢影响的近期研究，重点阐述潜在的调节机制。方法。总结了64项已发表的实验，这些实验将反式-10，顺式-12 CLA单独或与其他CLA异构体联合喂给小鼠、大鼠、仓鼠，并与人类进行比较。总结与结论。膳食反式-10，顺式-12 CLA可诱导小鼠发生严重的肝脂肪变性，而在其他物种中反应则较为轻微。无论物种如何，当出现肝脂肪变性时，同时会观察到体脂减少，这表明肝脏脂质积累是脂肪组织中动员的脂肪酸（FA）被摄取以及肝脏无法充分增加FA氧化和合成甘油三酯输出的结果。讨论了肝脏FA组成、胰岛素分泌和敏感性、脂肪因子以及炎症反应作为CLA诱导肝脂肪变性背后潜在机制的作用。
