Expression of porcine adipocyte transcripts: tissue distribution and differentiation in vitro and in vivo

被引:96
作者
Ding, ST [1 ]
McNeel, RL [1 ]
Mersmann, HJ [1 ]
机构
[1] Baylor Coll Med, Dept Pediat, USDA ARS, Childrens Nutr Res Ctr, Houston, TX 77030 USA
来源
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY B-BIOCHEMISTRY & MOLECULAR BIOLOGY | 1999年 / 123卷 / 03期
关键词
lipoprotein lipase; fatty acid binding protein; transcription factors; PPAR gamma; C/EBP alpha; RXR alpha; ADD1; adipocyte differentiation;
D O I
10.1016/S0305-0491(99)00077-2
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
Transcription factor transcripts implicated in adipocyte differentiation (peroxisome proliferator-activated receptor gamma (PPAR gamma), retinoid x receptor alpha (RXR alpha), adipocyte determination and differentiation-dependent factor 1 (ADD1), and CCAAT/enhancer binding protein alpha (C/EBP alpha)) and adipocyte-characteristic protein transcripts (lipoprotein lipase (LPL) and adipocyte fatty acid binding protein (aP2)) were measured in pig tissues. Transcripts for PPAR gamma, ADD1, and aP2 were localized in porcine subcutaneous and perirenal adipose tissues; transcripts for C/EBP alpha. and LPL were detected in other tissues, but the greatest concentrations were in the adipose tissues. In porcine stromal-vascular cells (S/V cells) differentiating in vitro, transcripts for PPAR gamma and aP2 increased gradually, transcripts for ADD1, and LPL increased early and transcripts for C/EBP alpha increased late. In pigs, adipose tissue transcripts for PPAR gamma, ADD1, and LPL were minimal at birth and increased to 28 days postpartum, transcripts for C/EBP alpha were low until 28 days and transcripts for aP2 were at high levels, regardless of age. Although transcript development was somewhat different in vitro and in vivo, the data suggest PPAR gamma land ADD1 are involved in regulation of transcripts for LPL and that there may be more partially differentiated precursor cells in S/V cells at day 0 than in adipose tissue at birth. (C) 1999 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:307 / 318
页数:12
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