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Reduction of phosphodiesterase 3B gene expression in peroxisome proliferator‐activated receptor γ (+/−) mice independent of adipocyte size
Author(s) -
Ogura Takahiro,
Osawa Haruhiko,
Tang Yan,
Onuma Hiroshi,
Ochi Masaaki,
Nishimiya Tatsuya,
Kubota Naoto,
Terauchi Yasuo,
Kadowaki Takashi,
Makino Hideichi
Publication year - 2003
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(03)00339-9
Subject(s) - peroxisome proliferator activated receptor , adipocyte , medicine , endocrinology , phosphodiesterase , receptor , gene expression , chemistry , insulin , peroxisome , biology , gene , adipose tissue , enzyme , biochemistry
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.