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Effects of phorbol ester‐sensitive PKC (c/nPKC) activation on the production of adiponectin in 3T3‐L1 adipocytes
Author(s) -
Ikeda Takahide,
Kajita Kazuo,
Zhiliang Wu,
Hanamoto Takayuki,
Mori Ichiro,
Fujioka Kei,
Okada Hideyuki,
Fujikake Takatoshi,
Uno Yoshihiro,
Morita Hiroyuki,
Nagano Isao,
Takahashi Yuzo,
Ishizuka Tatsuo
Publication year - 2009
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.193
Subject(s) - medicine , adipocyte , endocrinology , adiponectin , protein kinase c , insulin , chemistry , phorbol , peroxisome proliferator activated receptor , receptor , biology , adipose tissue , signal transduction , insulin resistance , biochemistry
PPARγ plays a key role in adipocyte specific gene expression. In this study, we assessed the effects of phorbol ester (TPA)‐sensitive PKC (c/nPKC) activation on the expression of adipocyte specific genes and inflammation related genes. Treatment with both TPA and TNFα decreased mRNA levels of PPARγ, aP2, LPL and adiponectin. TNFα, but not TPA, increased IL‐6 and MCP‐1 mRNA levels, Next, we investigated the effects of ligands which activate c/nPKC. Insulin and angiotensin II (AII), but not high glucose, reduced PPARγ, aP2 and adiponectin mRNA levels. AII‐induced suppression of these genes was restored in the presence of Go6976, a specific c/nPKC inhibitor, and candesartan, an AII receptor blocker. The effect of reduced insulin was prevented by Go6976 and LY294002, a specific PI 3‐kinase inhibitors. Our results indicate that activation of c/nPKC could debilitate and/or might deteriorate insulin sensitivity in vivo , through the reduction of PPARγ and adiponectin expression in adipocyte. © 2009 IUBMB IUBMB Life, 61(6): 644–650, 2009