PPARγ activators down‐regulate the expression of PPARγ in 3T3‐L1 adipocytes
Heidi S. Camp, Amy L Whitton, Sherrie Tafuri
Abstract
Heidi S. Camp, Amy L Whitton, Sherrie Tafuri
Abstract
Transcriptional activation of PPARgamma by the anti-diabetic compound troglitazone enhances the rate of 3T3-L1 adipocyte differentiation. In this study, we examined the effects of troglitazone, a specific PPARgamma ligand, on the expression of PPARgamma during and after 3T3-L1 adipocyte differentiation. Troglitazone treatment caused a significant decrease in PPARgamma proteins and DNA binding activity. This reduction was associated with a similar decrease in transcription of PPARgamma mRNA. These data suggest that in 3T3-L1 cells, the expression of PPARgamma is auto-regulated.
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Transcriptional activation of PPARgamma by the anti-diabetic compound troglitazone enhances the rate of 3T3-L1 adipocyte differentiation. In this study, we examined the effects of troglitazone, a specific PPARgamma ligand, on the expression of PPARgamma during and after 3T3-L1 adipocyte differentiation. Troglitazone treatment caused a significant decrease in PPARgamma proteins and DNA binding activity. This reduction was associated with a similar decrease in transcription of PPARgamma mRNA. These data suggest that in 3T3-L1 cells, the expression of PPARgamma is auto-regulated.
Key concepts: Troglitazone, Adipocyte, 3T3-L1, Peroxisome proliferator-activated receptor, Chemistry, Transcription factor, Internal medicine, Endocrinology