Flaxseed oil prevents trans-10, cis-12-conjugated linoleic acid-induced insulin resistance in mice
Flaxseed oil prevents trans-10, cis-12-conjugated linoleic acid-induced insulin resistance in mice
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DOI：
10.1017/s0007114508027451
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发表时间：
2009-03-14
影响因子：
3.6
通讯作者：
Mackey, Bruce E.
中科院分区：
文献类型：
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作者：
Kelley, Darshan S.;Vemuri, Madhuri;Mackey, Bruce E.
胰岛素抵抗（IR）和非酒精性脂肪肝（NAFLD）分别在35%和30%的美国成年人中发现。反式-10，顺式-12-共轭亚油酸（CLA）已被发现在几种动物模型中引起这两种疾病。我们推测CLA引起的IR和NAFLD是n-3脂肪酸缺乏的结果。无病原体的C57 BL/6 N雌性小鼠（8周龄; n 10）喂食对照饮食或含有反式-10，顺式-12-CLA（0.5%）或CLA +亚麻籽油（FSO）（0.5% ± 0.5%）的饮食8周。CLA组肝脏重量、循环胰岛素浓度、IR稳态模型1（HOMA 1）值和0细胞功能HOMA 1值分别比对照组高160、636、985和968%。与CLA组相比，FSO使空腹血糖降低了20%，肝脏重量降低了37%;它使循环胰岛素、HOMA 1-IR和HOMA 1的P细胞功能保持在对照组的水平。与对照组的相应值相比，CLA补充使肝脏脂质的n-6和n-3重量%浓度降低了57%和73%，并使n-6：n-3比率增加了58%。与CLA组的相应值相比，FSO使肝脏脂质中的n-6和n-3 PUFA增加了33%和342%，并使n-6：n-3比率降低了70%。目前的研究结果表明，CLA的一些不良影响可能是由于n-3 PUFA缺乏，这些可以通过同时增加α-亚麻酸，18：3 n-3的摄入量来纠正。
Insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD) are found in 35 and 30% of US adults, respectively. Trans-10, cis-12-conjugated linoleic acid (CLA) has been found to cause both these disorders in several animal models. We hypothesised that IR and NAFLD caused by CLA result from n-3 fatty acid deficiency. Pathogen-free C57BL/6N female mice (aged 8 weeks; n 10) were fed either a control diet or diets containing trans-10, cis-12-CLA (0.5 %) or CLA + flaxseed oil (FSO) (0.5 % + 0.5 %) for 8 weeks. Weights of livers, concentration of circulating insulin, values of homeostatic model 1 (HOMA1) for IR and HOMA1 for 0 cell function were higher by 160, 636, 985 and 968 % in the CLA group compared with those in the control group. FSO decreased fasting glucose by 20 % and liver weights by 37 % compared with those in the CLA group; it maintained circulating insulin, HOMA1-IR and HOMA1 for P cell function at levels found in the control group. CLA supplementation decreased n-6 and n-3 wt% concentrations of liver lipids by 57 and 73 % and increased the n-6:n-3 ratio by 58 % compared with corresponding values in the control group. FSO increased n-6 and n-3 PUFA in liver lipids by 33 and 342 % and decreased the n-6:n-3 ratio by 70 % compared with corresponding values in the CLA group. The present results suggest that some adverse effects of CLA may be due to n-3 PUFA deficiency and that these can be corrected by a concomitant increase in the intake of a-linolenic acid, 18: 3n-3.