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多不饱和脂肪酸对肥胖小鼠的影响。

Effect of polyunsaturated fatty acids in obese mice.

作者信息

Clandinin M T, Cheema S, Pehowich D, Field C J

机构信息

Department of Agricultural, Food, and Nutritional Science, University of Alberta, Edmonton, Canada.

出版信息

Lipids. 1996 Mar;31 Suppl:S13-22. doi: 10.1007/BF02637045.

Abstract

Genetically obese (ob/ob) mice display a variety of metabolic differences from lean litter mates. In the obese state, fatty acid desaturation-elongation in brown adipose tissue mitochondria is apparently altered, resulting in differences in membrane fatty acid composition. This change in membrane lipid environment appears to influence GDP binding and therefore the activity of the proton conductance pathway associated with regulation of energy expenditure in these animals. In liver, binding of insulin to the nuclear membrane is increased by feeding a high polyunsaturated/saturated (P/S) diet fat. Consumption of a high P/S diet decreased mRNA levels for fatty acid synthase, acetyl-CoA carboxylase, malic enzyme, and pyruvate kinase in obese and lean animals. Expression of mRNA for these lipogenic enzymes was higher in obese animals and suggests that obese mice may be resistant to polyunsaturated fatty acid feedback control of gene expression.

摘要

基因肥胖(ob/ob)小鼠与同窝瘦小鼠表现出多种代谢差异。在肥胖状态下,棕色脂肪组织线粒体中的脂肪酸去饱和-延长过程明显改变,导致膜脂肪酸组成存在差异。膜脂质环境的这种变化似乎会影响GDP结合,进而影响与这些动物能量消耗调节相关的质子传导途径的活性。在肝脏中,通过喂食高多不饱和/饱和(P/S)饮食脂肪,胰岛素与核膜的结合会增加。食用高P/S饮食会降低肥胖和瘦小鼠中脂肪酸合酶、乙酰辅酶A羧化酶、苹果酸酶和丙酮酸激酶的mRNA水平。这些生脂酶的mRNA在肥胖小鼠中表达较高,这表明肥胖小鼠可能对多不饱和脂肪酸对基因表达的反馈控制具有抗性。

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