Diet-induced insulin resistance in mice lacking adiponectin/ACRP30

被引:1680
|
作者
Maeda, N
Shimomura, I
Kishida, K
Nishizawa, H
Matsuda, M
Nagaretani, H
Furuyama, N
Kondo, H
Takahashi, M
Arita, Y
Komuro, R
Ouchi, N
Kihara, S
Tochino, Y
Okutomi, K
Horie, M
Takeda, S
Aoyama, T
Funahashi, T
Matsuzawa, Y
机构
[1] Osaka Univ, Grad Sch Med, Dept Internal Med & Mol Sci, Osaka, Japan
[2] Otsuka Pharmaceut Co Ltd, Otsuga GEN Res Inst, Tokushima 77101, Japan
[3] Shinshu Univ, Sch Med, Dept Aging Biochem, Nagano, Japan
基金
日本学术振兴会;
关键词
D O I
10.1038/nm724
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Here we investigated the biological functions of adiponectin/ACRP30, a fat-derived hormone, by disrupting the gene that encodes it in mice. Adiponectin/ACRP30-knockout (KO) mice showed delayed clearance of free fatty acid in plasma, low levels of fatty-acid transport protein 1 (FATP-1) mRNA in muscle, high levels of tumor necrosis factor-alpha (TNF-alpha) mRNA in adipose tissue and high plasma TNF-alpha concentrations. The KO mice exhibited severe diet-induced insulin resistance with reduced insulin-receptor substrate 1 (IRS-1)-associated phosphatidylinositol 3 kinase (PI3-kinase) activity in muscle. Viral mediated adiponectin/ACRP30 expression in KO mice reversed the reduction of FATP-1 mRNA, the increase of adipose TNF-alpha mRNA and the diet-induced insulin resistance. In cultured myocytes, TNF-alpha decreased FATP-1 mRNA, IRS-1-associated PI3-kinase activity and glucose uptake, whereas adiponectin increased these parameters. Our results indicate that adiponectin/ACRP30 deficiency and high TNF-alpha levels in KO mice reduced muscle FATP-1 mRNA and IRS-1-mediated insulin signaling, resulting in severe diet-induced insulin resistance.
引用
收藏
页码:731 / 737
页数:7
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