한빛사 논문
Chang-Myung Oh1,*, Jun Namkung1,2,*, Younghoon Go3,*, Ko Eun Shong1, Kyuho Kim1, Hyeongseok Kim1, Bo-Yoon Park3,4, Ho Won Lee5, Yong Hyun Jeon5,6, Junghan Song7, Minho Shong8, Vijay K. Yadav9, Gerard Karsenty10, Shingo Kajimura11, In-Kyu Lee3,4, Sangkyu Park1,12 & Hail Kim1
1 BioMedical Research Center (E7) 8104, Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea. 2 Department of Biochemistry, Yonsei University Wonju College of Medicine, Wonju 220-701, Korea. 3 Department of Internal Medicine, Kyungpook National University Hospital, Kyungpook National University School of Medicine, Daegu 700-721, Korea. 4 BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University Hospital, Kyungpook National University School of Medicine, Daegu 700-842, Korea. 5 Department of Nuclear Medicine, Kyungpook National University Hospital, Kyungpook National University School of Medicine, Daegu 700-721, Korea. 6 Leading-edge Research Center for Drug Discovery and Development for Diabetes and Metabolic Disease, Kyungpook National University Hospital, Kyungpook National University School of Medicine, Daegu 702-210, Korea. 7 Department of Laboratory Medicine, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seoul 463-707, Korea. 8 Research Center for Endocrine and Metabolic Diseases, Chungnam National University School of Medicine, Daejeon 301-721, Korea. 9Wellcome Trust Sanger Institute, Cambridge CB10 1SA, UK. 10 Department of Genetics and Development, Columbia University Medical Center, New York, New York 10032, USA. 11 Diabetes Center, Hormone Research Institute and Department of Medicine, University of California San Francisco, San Francisco, California 94143, USA. 12 Department of Biochemistry, College of Medicine, Catholic Kwandong University, Gangneung 210-701, Korea.
* These authors contributed equally to this work as first authors.
Correspondence to : In-Kyu Lee or Sangkyu Park or Hail Kim
Abstract
Central serotonin (5-HT) is an anorexigenic neurotransmitter in the brain. However, accumulating evidence suggests peripheral 5-HT may affect organismal energy homeostasis. Here we show 5-HT regulates white and brown adipose tissue function. Pharmacological inhibition of 5-HT synthesis leads to inhibition of lipogenesis in epididymal white adipose tissue (WAT), induction of browning in inguinal WAT and activation of adaptive thermogenesis in brown adipose tissue (BAT). Mice with inducible Tph1 KO in adipose tissues exhibit a similar phenotype as mice in which 5-HT synthesis is inhibited pharmacologically, suggesting 5-HT has localized effects on adipose tissues. In addition, Htr3a KO mice exhibit increased energy expenditure and reduced weight gain when fed a high-fat diet. Treatment with an Htr2a antagonist reduces lipid accumulation in 3T3-L1 adipocytes. These data suggest important roles for adipocyte-derived 5-HT in controlling energy homeostasis.
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