Abstract
Phosphodiesterase 3B (PDE3B) gene expression is generally reduced in large adipocytes of obese, insulin-resistant mice. This reduced gene expression is restored by peroxisome proliferator-activated receptor (PPAR) γ ligands accompanied by a reduced fat cell size. To determine whether PDE3B gene expression is regulated by PPARγ itself, we analyzed lean PPARγ (+/-) mice with adipocyte size comparable to control PPARγ (+/+) mice. In adipocytes of PPARγ (+/-) mice, PDE3B mRNA and protein were both reduced to 63% of wild-type levels. Basal PDE activity tended to be decreased to 70% of wild-type levels, and, similarly, insulin-induced PDE activity was significantly decreased to 70%. Thus, PPARγ is required for PDE3B gene expression independent of adipocyte size.
Original language | English (US) |
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Pages (from-to) | 65-68 |
Number of pages | 4 |
Journal | FEBS Letters |
Volume | 542 |
Issue number | 1-3 |
DOIs | |
State | Published - May 8 2003 |
Externally published | Yes |
Keywords
- Adipocyte
- Insulin
- Insulin resistance
- Peroxisome proliferator-activated receptor γ
- Phosphodiesterase 3B
- Type 2 diabetes
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology