Regulation of adipocyte differentiation and function by polyunsaturated fatty acids

被引:219
作者
Madsen, L
Petersen, RK
Kristiansen, K
机构
[1] Univ So Denmark, Dept Biochem & Mol Biol, DK-5230 Odense, Denmark
[2] BioLigands, Odense, Denmark
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2005年 / 1740卷 / 02期
关键词
polyunsaturated fatty acid; adipocyte differentiation; peroxisome proliferator-activated receptor; sterol regulatory element-binding protein; liver X receptor;
D O I
10.1016/j.bbadis.2005.03.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
A diet enriched in PUFAs, in particular of the n-3 family, decreases adipose tissue mass and suppresses development of obesity in rodents. Although several nuclear hormone receptors are identified as PUFA targets, the precise molecular mechanisms underlying the effects of PUFAs still remain to be elucidated. Here we review research aimed at elucidating molecular mechanisms governing the effects of PUFAs on the differentiation and function of white fat cells. This review focuses on dietary PUFAs as signaling molecules, with special emphasis on agonistic and antagonistic effects on transcription factors currently implicated as key players in adipocyte differentiation and function, including peroxisome proliferator activated receptors (PPARs) (alpha, beta and gamma), sterol regulatory element binding proteins (SREBPs) and liver X receptors (LXRs). We review evidence that dietary n-3 PUFAs decrease adipose tissue mass and Suppress the development of obesity in rodents by targeting a set of key regulatory transcription factors involved in both adipogensis and lipid homeostasis in mature adipocytes. The same set of factors are targeted by PUFAs of the n-6 family, but the cellular/physiological responses are dependent on the experimental setting as n-6 PUFAs may exert either an anti- or a proadipogenic effect. Feeding status and hormonal background may therefore be of particular importance in determining the physiological effects of PUFAs of the n-6 family. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:266 / 286
页数:21
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