Adipocyte-specific reduction of phosphodiesterase 3B gene expression and its restoration by JTT-501 in the obese, diabetic KKAy mouse
Author(s) -
Yan Tang,
Haruhiko Osawa,
Hiroshi Onuma,
Masaaki Hasegawa,
Tatsuya Nishimiya,
Masayuki Ochi,
Hideichi Makino
Publication year - 2001
Publication title -
european journal of endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.897
H-Index - 148
eISSN - 1479-683X
pISSN - 0804-4643
DOI - 10.1530/eje.0.1450093
Subject(s) - medicine , endocrinology , adipose tissue , phosphodiesterase , insulin resistance , pioglitazone , adipocyte , insulin , gene expression , thiazolidinedione , biology , diabetes mellitus , enzyme , type 2 diabetes , gene , biochemistry
Phosphodiesterase (PDE) 3B is a key enzyme involved in the anti-lipolytic action of insulin in adipocytes. PDE3B activation results in a reduced output of free fatty acids (FFA), whereas elevated serum FFA is known to cause insulin resistance. We have recently reported that reduced PDE3B gene expression is restored by treatment with pioglitazone, in the adipose tissues of obese, insulin-resistant diabetic KKAy mice. To determine whether the altered PDE3B gene expression is specific for adipocytes, the expression of this gene in liver and epididymal fat tissues of KKAy mice was examined. The effect of JTT-501, another peroxisome proliferator-activated receptor (PPAR)gamma ligand, which is different from thiazolidinedione, was also examined.
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