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Article
Nature Medicine 10, 727 - 733 (2004)
Published online: 13 June 2004; Corrected online: 20  2004 | doi:10.1038/nm1061

Anti-obesity effects of alpha-lipoic acid mediated by suppression of hypothalamic AMP-activated protein kinase

Min-Seon Kim1, Joong-Yeol Park1, Cherl Namkoong2, Pil-Geum Jang2, Je-Won Ryu2, Hai-Sun Song2, Ji-Young Yun2, Il-Seong Namgoong1, Joohun Ha3, In-Sun Park4, In-Kyu Lee5, Benoit Viollet6, Jang Hyun Youn7, Hong-Kyu Lee8 & Ki-Up Lee1

1  Department of Internal Medicine, University of Ulsan College of Medicine, 138-736 Poongnap-dong, Songpa-ku, Seoul 138-736, Korea.

2  Asan Institute for Life Sciences, University of Ulsan College of Medicine, 138-736 Poongnap-dong, Songpa-ku, Seoul 138-736, Korea.

3  Department of Molecular Biology, Kyunghee University College of Medicine, 1 Hoegi-dong Tongdaemun-gu, Seoul 130-701, Korea.

4  Department of Anatomy, College of Medicine, Inha University, 7-241 Shinheung-dong, Choong-ku, Incheon 400-103, Korea.

5  Department of Internal Medicine, Keimyung University School of Medicine, 194 Dongsan-dong, Taegu 700-310, Korea.

6  Department of Genetics, Development and Molecular Pathology, Institut Cochin, INSERM, CNRS, Rene Descartes University, 24 rue du Faubourg Saint-Jacques, 75014 Paris, France.

7  Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, 1333 San Pablo St. MMR626, Los Angeles, CA 90089, USA.

8  Department of Internal Medicine, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-ku, Seoul 110-744, Korea.

Correspondence should be addressed to Ki-Up Lee kulee@amc.seoul.kr

AMP-activated protein kinase (AMPK) functions as a fuel sensor in the cell and is activated when cellular energy is depleted. Here we report that alpha-lipoic acid (alpha-LA), a cofactor of mitochondrial enzymes, decreases hypothalamic AMPK activity and causes profound weight loss in rodents by reducing food intake and enhancing energy expenditure. Activation of hypothalamic AMPK reverses the effects of alpha-LA on food intake and energy expenditure. Intracerebroventricular (i.c.v.) administration of glucose decreases hypothalamic AMPK activity, whereas inhibition of intracellular glucose utilization through the administration of 2-deoxyglucose increases hypothalamic AMPK activity and food intake. The 2-deoxyglucose-induced hyperphagia is reversed by inhibiting hypothalamic AMPK. Our findings indicate that hypothalamic AMPK is important in the central regulation of food intake and energy expenditure and that alpha-LA exerts anti-obesity effects by suppressing hypothalamic AMPK activity.
NOTE: In the version of this article initially published online, the name of an author was misspelled. The name of the twelfth author should be "Benoit Viollet". This error has been corrected for the HTML and print versions of the article

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ISSN: 1078-8956
EISSN: 1546-170X
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