Abstract:
: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.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Aubert J,Champigny O,Saint-Marc P,Negrel R,Collins S,Ricquier D,Ailhaud Gdoi
10.1006/bbrc.1997.7348subject
Has Abstractpub_date
1997-09-18 00:00:00pages
606-11issue
2eissn
0006-291Xissn
1090-2104pii
S0006-291X(97)97348-4journal_volume
238pub_type
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