Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Transcriptional Regulation of Gene Expression During Adipocyte Differentiation

Transcriptional Regulation of Gene Expression During Adipocyte Differentiation STAGE·SPECIFIC GENE EXPRESSION DURING ADIPOCYTE DEVELOMENT .. ABSTRACf Cell culture models (e.g. 3T3-L1 cells) have been developed for studying the process of adipocyte differentiation. Differentiation can be induced by adding insulin-like growth factor I, glucocorticoid, fatty acids, and an agent that increases intracellular cAMP level. The adipocyte differentiation program is regulated by transcriptional activators such as CCAAT/enhancer binding pro­ teina (CIEBPa), peroxisomal proliferator activated receptor y2 (PPARy2), fatty acid activated receptor (FAAR), and transcriptional repressors such as preadipocyte repressor element binding protein (PRE) and CIEBP undifferen­ tiated protein (CUP). These transcription factors coordinate the expression of genes involved in creating and maintaining the adipocyte phenotype including the insulin-responsive glucose transporter (GLUT4), stearoyl CoA desaturase 1 (SCDl), and the fatty acid binding protein (4 2 21aP2). PERSPECTIVES AND SUMMARY Adipocytes serve an important function in the energy economy of vertebrate organisms by providing a massive energy reserve that can be mobilized upon demand. Thus, when caloric intake exceeds expenditure, metabolic flux is directed into pathways leading to triacylglycerol synthesis for storage in the adipocyte. Conversely, when caloric expenditure exceeds intake, this energy reserve is mobilized to meet the deficiency and to provide needed physiological fuel, i.e. free fatty acids, http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Biochemistry Annual Reviews

Transcriptional Regulation of Gene Expression During Adipocyte Differentiation

MacDougald, O A; Lane, M D
Annual Review of Biochemistry , Volume 64 (1) – Jul 1, 1995
Download PDF
29 pages

Loading next page...
 
/lp/annual-reviews/transcriptional-regulation-of-gene-expression-during-adipocyte-zrdtSG63qF

References

References for this paper are not available at this time. We will be adding them shortly, thank you for your patience.

Publisher
Annual Reviews
Copyright
Copyright 1995 Annual Reviews. All rights reserved
Subject
Review Articles
ISSN
0066-4154
eISSN
1545-4509
DOI
10.1146/annurev.bi.64.070195.002021
pmid
7574486
Publisher site
See Article on Publisher Site

Abstract

STAGE·SPECIFIC GENE EXPRESSION DURING ADIPOCYTE DEVELOMENT .. ABSTRACf Cell culture models (e.g. 3T3-L1 cells) have been developed for studying the process of adipocyte differentiation. Differentiation can be induced by adding insulin-like growth factor I, glucocorticoid, fatty acids, and an agent that increases intracellular cAMP level. The adipocyte differentiation program is regulated by transcriptional activators such as CCAAT/enhancer binding pro­ teina (CIEBPa), peroxisomal proliferator activated receptor y2 (PPARy2), fatty acid activated receptor (FAAR), and transcriptional repressors such as preadipocyte repressor element binding protein (PRE) and CIEBP undifferen­ tiated protein (CUP). These transcription factors coordinate the expression of genes involved in creating and maintaining the adipocyte phenotype including the insulin-responsive glucose transporter (GLUT4), stearoyl CoA desaturase 1 (SCDl), and the fatty acid binding protein (4 2 21aP2). PERSPECTIVES AND SUMMARY Adipocytes serve an important function in the energy economy of vertebrate organisms by providing a massive energy reserve that can be mobilized upon demand. Thus, when caloric intake exceeds expenditure, metabolic flux is directed into pathways leading to triacylglycerol synthesis for storage in the adipocyte. Conversely, when caloric expenditure exceeds intake, this energy reserve is mobilized to meet the deficiency and to provide needed physiological fuel, i.e. free fatty acids,

Journal

Annual Review of Biochemistry – Annual Reviews

Published: Jul 1, 1995

There are no references for this article.