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人体中的共轭亚油酸:对肥胖和胰岛素敏感性的调节

Conjugated linoleic acid in humans: regulation of adiposity and insulin sensitivity.

作者信息

Brown J Mark, McIntosh Michael K

机构信息

Department of Nutrition, University of North Carolina at Greensboro, Greensboro, NC 27402-6170, USA.

出版信息

J Nutr. 2003 Oct;133(10):3041-6. doi: 10.1093/jn/133.10.3041.

Abstract

Conjugated linoleic acid (CLA) isomers, a group of positional and geometric isomers of linoleic acid [18:2(n-6)], have been studied extensively due to their ability to modulate cancer, atherosclerosis, obesity, immune function and diabetes in a variety of experimental models. The purpose of this review was to examine CLA's isomer-specific regulation of adiposity and insulin sensitivity in humans and in cultures of human adipocytes. It has been clearly demonstrated that specific CLA isomers or a crude mixture of CLA isomers prevent the development of obesity in certain rodent and pig models. This has been attributed mainly to trans-10, cis-12 CLA, both in vivo and in vitro. However, CLA's ability to modulate human obesity remains controversial because data from clinical trials using mixed isomers are conflicting. In support of some studies in humans, our group demonstrated that trans-10, cis-12 CLA prevents triglyceride (TG) accumulation in primary cultures of differentiating human preadipocytes. In contrast, cis-9, trans-11 CLA increases TG content. Closer examination has revealed that CLA's antiadipogenic actions are due, at least in part, to regulation of glucose and fatty acid uptake and metabolism. This review presents our current understanding of potential isomer-specific mechanisms by which CLA reduces human adiposity and insulin sensitivity.

摘要

共轭亚油酸(CLA)异构体是亚油酸[18:2(n-6)]的一组位置和几何异构体,由于它们能够在多种实验模型中调节癌症、动脉粥样硬化、肥胖、免疫功能和糖尿病,因此受到了广泛研究。本综述的目的是研究CLA对人类和人脂肪细胞培养物中肥胖和胰岛素敏感性的异构体特异性调节作用。已经清楚地证明,特定的CLA异构体或CLA异构体的粗混合物可预防某些啮齿动物和猪模型中的肥胖症发展。这主要归因于体内和体外的反式-10,顺式-12 CLA。然而,CLA调节人类肥胖的能力仍存在争议,因为使用混合异构体的临床试验数据相互矛盾。为了支持一些对人类的研究,我们小组证明反式-10,顺式-12 CLA可防止分化中的人前脂肪细胞原代培养物中甘油三酯(TG)的积累。相比之下,顺式-9,反式-11 CLA会增加TG含量。进一步研究发现,CLA的抗脂肪生成作用至少部分归因于对葡萄糖和脂肪酸摄取及代谢的调节。本综述介绍了我们目前对CLA降低人类肥胖和胰岛素敏感性的潜在异构体特异性机制的理解。

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