PPARγ is a member of the nuclear hormone receptor superfamily and functions as a transcriptional regulator of genes linked to adipogenesis and lipid metabolism. The regulation of PPARγ activity by insulin signaling molecules in adipocytes has yet to be clarified. Therefore, it is important to measure endogenous PPARγ transcriptional activities in response to various stimuli in adipocytes. Herein, with a transcription reporter assay using recombinant adenovirus vectors expressing PPRE (PPAR responsive elements)-reporter genes, we established a novel system for measuring endogenous PPARγ transcriptional activity in 3T3-L1 adipocytes. By means of this system, a marked increase (8.5-fold) in PPARγ transcriptional activity was detected after treatment with 10-6M pioglitazone, a thiazolidinedione (TZD), indicating that this system can measure PPARγ activity accurately. Furthermore, MAPK activation, achieved by overexpressing constitutively activated MEK1, inhibited PPARγ transcriptional activity. In contrast, treatment with PKA stimulators markedly increased PPARγ activity. Interestingly, PI 3-kinase overexpression resulted in a marked decrease in PPARγ activity. These observations have important implications for understanding the regulation of PPARγ transcriptional activity.
|ジャーナル||Biochemical and biophysical research communications|
|出版ステータス||Published - 2003 1 10|
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