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J. Biol. Chem., Vol. 281, Issue 13, 8748-8755, March 31, 2006
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Pioglitazone Ameliorates Insulin Resistance and Diabetes by Both Adiponectin-dependent and -independent Pathways*
¶¶¶¶1
From the
Department of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, the CREST of Japan Science and Technology Agency, Saitama, 332-0012, the ¶Division of Applied Nutrition, National Institute of Health and Nutrition, Tokyo 162-8636, the ||Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tsukuba 305-0006, the **Division of Cardiovascular Medicine, Toho University, Ohashi Hospital, Tokyo 153-8515, the Department of Cell Biology, Japanese Foundation for Cancer Research-Cancer Institute, Tokyo 135-8550, the Department of Molecular Genetics, Tohoku University School of Medicine, Sendai 980-8575, and the ¶¶Department of Cardiovascular Diseases, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan
*Thiazolidinediones have been shown to up-regulate adiponectin expression in white adipose tissue and plasma adiponectin levels, and these up-regulations have been proposed to be a major mechanism of the thiazolidinedione-induced amelioration of insulin resistance linked to obesity. To test this hypothesis, we generated adiponectin knock-out (adipo-/-) ob/ob mice with a C57B/6 background. After 14 days of 10 mg/kg pioglitazone, the insulin resistance and diabetes of ob/ob mice were significantly improved in association with significant up-regulation of serum adiponectin levels. Amelioration of insulin resistance in ob/ob mice was attributed to decreased glucose production and increased AMP-activated protein kinase in the liver but not to increased glucose uptake in skeletal muscle. In contrast, insulin resistance and diabetes were not improved in adipo-/-ob/ob mice. After 14 days of 30 mg/kg pioglitazone, insulin resistance and diabetes of ob/ob mice were again significantly ameliorated, which was attributed not only to decreased glucose production in the liver but also to increased glucose uptake in skeletal muscle. Interestingly, adipo-/-ob/ob mice also displayed significant amelioration of insulin resistance and diabetes, which was attributed to increased glucose uptake in skeletal muscle but not to decreased glucose production in the liver. The serum-free fatty acid and triglyceride levels as well as adipocyte sizes in ob/ob and adipo-/-ob/ob mice were unchanged after 10 mg/kg pioglitazone but were significantly reduced to a similar degree after 30 mg/kg pioglitazone. Moreover, the expressions of TNF
and resistin in adipose tissues of ob/ob and adipo-/-ob/ob mice were unchanged after 10 mg/kg pioglitazone but were decreased after 30 mg/kg pioglitazone. Thus, pioglitazone-induced amelioration of insulin resistance and diabetes may occur adiponectin dependently in the liver and adiponectin independently in skeletal muscle.
Received for publication, May 23, 2005 , and in revised form, December 7, 2005.
* This work was supported by a grant from the Program for Promotion of Fundamental Studies in Health Sciences of the Organization for Pharmaceutical Safety and Research of Japan, a grant-in-aid for the Development of Innovative Technology from the Ministry of Education, Culture, Sports, Science and Technology (to T. K.), and by Health Science Research Grants (Research on Human Genome and Gene Therapy) from the Ministry of Health and Welfare (to T. K.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 To whom correspondence should be addressed: Dept. of Metabolic Diseases, Graduate School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. Tel.: 81-3-5800-8815; Fax: 81-3-5800-9797; E-mail: kadowaki-3im{at}h.u-tokyo.ac.jp.
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