Up-regulation of UCP-2 gene expression by PPAR agonists in preadipose and adipose cells.

Journal Article (Journal Article)

UCP-2 is a member of the emerging family of UCP homologues. Upon high-fat feeding, UCP-2 mRNA levels are increased in epididymal fat pads of A/J mice, suggesting that the flux of fatty acids entering adipose tissue may regulate UCP-2 gene expression. Since fatty acids act as positive transcriptional regulators of lipid-related genes by means of peroxisome proliferator-activated receptors (PPARs), the regulation of UCP-2 gene expression by PPAR agonists (carbacyclin, alpha-bromopalmitate, BRL49653) has been examined in mouse preadipose and adipose cells in primary cultures or from clonal lines (Ob1771, 3T3-F442A, 1B8). In preadipose cells, carbacyclin and alpha-bromopalmitate are active and BRL49653 shows no effect, whereas all these ligands are active in adipose cells. The stimulatory effect of PPAR agonists is potentiated by RXR agonists in adipose cells. In contrast to the UCP-1 gene, norepinephrine as a cAMP-elevating agent does not enhance the expression of UCP-2 gene. Altogether, the data favor a predominant role of PPARdelta in preadipose cells and the involvement of PPARgamma2 in adipose cells in up-regulating UCP-2 gene expression. Thus, a potential link between fatty acid metabolism and thermogenesis may exist in PPAR-expressing tissues.

Full Text

Duke Authors

Cited Authors

  • Aubert, J; Champigny, O; Saint-Marc, P; Negrel, R; Collins, S; Ricquier, D; Ailhaud, G

Published Date

  • September 18, 1997

Published In

Volume / Issue

  • 238 / 2

Start / End Page

  • 606 - 611

PubMed ID

  • 9299560

International Standard Serial Number (ISSN)

  • 0006-291X

Digital Object Identifier (DOI)

  • 10.1006/bbrc.1997.7348


  • eng

Conference Location

  • United States