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Coordinated control of energy metabolism and glucose homeostasisrequires communication between organs and tissues. We identifieda neuronal pathway that participates in the cross talk betweenthe liver and adipose tissue. By studying a mouse model, weshowed that adenovirus-mediated expression of peroxisome proliferator–activatedreceptor (PPAR)–g2 in the liver induces acute hepaticsteatosis while markedly decreasing peripheral adiposity. Thesechanges were accompanied by increased energy expenditure andimproved systemic insulin sensitivity. Hepatic vagotomy andselective afferent blockage of the hepatic vagus revealed thatthe effects on peripheral tissues involve the afferent vagalnerve. Furthermore, an antidiabetic thiazolidinedione, a PPARgagonist, enhanced this pathway. This neuronal pathway from theliver may function to protect against metabolic perturbationinduced by excessive energy storage.
1 Division of Molecular Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai 980–8575, Japan. 2 Advanced Therapeutics for Metabolic Diseases, Center for Translational and Advanced Animal Research, Tohoku University Graduate School of Medicine, Sendai 980–8575, Japan. 3 Department of Pathology, Tohoku University Graduate School of Medicine, Sendai 980–8575, Japan. 4 The Fourth Department of Internal Medicine, Saitama Medical School, Moroyama, Iruma-gun, Saitama 350–0495, Japan. 5 Laboratory of Gene Transfer and Regulation, National Institute of Biomedical Innovation, Osaka 567–0085, Japan. 6 Department of Physiological Chemistry and Metabolism, University of Tokyo, Tokyo 113–8655, Japan. 7 Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN 37232, USA. 8 Third Department of Internal Medicine, Miyazaki Medical College, University of Miyazaki, Kiyotake, Miyazaki 889–1692, Japan.
* These authors contributed equally to this work.
To whom correspondence should be addressed E-mail: katagiri{at}mail.tains.tohoku.ac.jp
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