CD36 promotes adipocyte differentiation and adipogenesis

被引:109
作者
Christiaens, Valerie [1 ]
Van Hul, Matthias [1 ]
Lijnen, H. Roger [1 ]
Scroyen, Ilse [1 ]
机构
[1] Katholieke Univ Leuven, Ctr Mol & Vasc Biol, B-3000 Louvain, Belgium
来源
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS | 2012年 / 1820卷 / 07期
关键词
(Pre)adipocyte; Adipogenesis; Adipose tissue; CD36; CHAIN FATTY-ACIDS; ADIPOSE-TISSUE DEVELOPMENT; SCAVENGER RECEPTOR; INSULIN-RESISTANCE; FUNCTIONAL-ROLE; INDUCED OBESITY; MICE; COLLAGEN; CELLS; ANGIOGENESIS;
D O I
10.1016/j.bbagen.2012.04.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Background: CD36 is a membrane glycoprotein, contributing to the pathogenesis of metabolic disorders, like obesity, which has become a major health concern worldwide. Methods: A potential functional role of the scavenger receptor CD36 was investigated in in vitro adipocyte differentiation and in vivo adipogenesis. Results: During differentiation of 3T3-F442A preadipocytes into mature adipocytes, expression of CD36 was upregulated and CD36 gene silencing resulted in impaired differentiation, as monitored by Oil Red 0 staining and expression of adipogenic markers. De novo fat pad formation in NUDE mice following injection of preadipocytes was significantly reduced upon CD36 gene silencing as compared to control. This was associated with marked adipocyte hypotrophy and reduced adipose tissue adipocyte content. Macrophage infiltration in de novo fat tissues derived from preadipocytes with CD36 gene silencing was not significantly different from controls. Collagen content was significantly higher in de novo fat with CD36 gene silencing. In a nutritionally induced obesity model, total body weight as well as subcutaneous and gonadal adipose tissue mass were significantly lower in CD36 deficient mice as compared to wild-type littermates. General significance: Thus, our data support a functional role of CD36 in promoting adipogenesis in vitro as well as in vivo. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:949 / 956
页数:8
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