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Article
Nature Medicine  10, 1208 - 1215 (2004)
Published online: 17 October 2004; | doi:10.1038/nm1117


There is a Retraction (June 2005) associated with this Article.

Enhanced insulin sensitivity, energy expenditure and thermogenesis in adipose-specific Pten suppression in mice

Nobuyasu Komazawa1, Morihiro Matsuda2, Gen Kondoh1, Wataru Mizunoya3, Masanori Iwaki2, Toshiyuki Takagi2, Yasuyuki Sumikawa4, Kazuo Inoue3, Akira Suzuki5, Tak Wah Mak6, Toru Nakano7, Tohru Fushiki3, Junji Takeda1, 8 & Iichiro Shimomura2, 9, 10

1  Department of Social and Environmental Medicine, Graduate School of Frontier Bioscience, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871.

2  Department of Medicine and Pathophysiology, Graduate School of Frontier Bioscience, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871.

3  Laboratory of Nutrition Chemistry, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Kitashirakawa, Sakyo-ku, Kyoto, 606-8502.

4  Department of Dermatology, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871.

5  Department of Biochemistry, Akita University, 1-1 Hondou, Akita, Akita, 010-8543, Japan.

6  Advanced Medical Discovery Institute, University of Toronto, Toronto, Ontario M5G 2Cl, Canada.

7  Department of Pathology, Graduate School of Medicine, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871

8  Center for Advanced Science and Innovation, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871

9  Department of Internal Medicine and Molecular Science, Osaka University, 2-2 Yamadaoka, Suita, Osaka 565-0871.

10  PREST, Japan Science and Technology Agency, 4-1-8 Honcho, Kawaguchi, Saitama 332-0012, Japan.

Correspondence should be addressed to Iichiro Shimomura ichi@imed2.med.osaka-u.ac.jp
Pten is an important phosphatase, suppressing the phosphatidylinositol-3 kinase/Akt pathway. Here, we generated adipose-specific Pten-deficient (AdipoPten-KO) mice, using newly generated Acdc promoter−driven Cre transgenic mice. AdipoPten-KO mice showed lower body and adipose tissue weights despite hyperphagia and enhanced insulin sensitivity with induced phosphorylation of Akt in adipose tissue. AdipoPten-KO mice also showed marked hyperthermia and increased energy expenditure with induced mitochondriagenesis in adipose tissue, associated with marked reduction of p53, inactivation of Rb, phosphorylation of cyclic AMP response element binding protein (CREB) and increased expression of Ppargc1a, the gene that encodes peroxisome proliferative activated receptor gamma coactivator 1 alpha. Physiologically, adipose Pten mRNA decreased with exposure to cold and increased with obesity, which were linked to the mRNA alterations of mitochondriagenesis. Our results suggest that altered expression of adipose Pten could regulate insulin sensitivity and energy expenditure. Suppression of adipose Pten may become a beneficial strategy to treat type 2 diabetes and obesity.

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Nature Medicine
ISSN: 1078-8956
EISSN: 1546-170X
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