Cyclooxygenase-2 Controls Energy Homeostasis in Mice by de Novo Recruitment of Brown Adipocytes

Author:

Vegiopoulos Alexandros1,Müller-Decker Karin2,Strzoda Daniela1,Schmitt Iris1,Chichelnitskiy Evgeny1,Ostertag Anke1,Diaz Mauricio Berriel1,Rozman Jan3,Hrabe de Angelis Martin3,Nüsing Rolf M.4,Meyer Carola W.5,Wahli Walter6,Klingenspor Martin7,Herzig Stephan1

Affiliation:

1. Emmy Noether and Marie Curie Research Group Molecular Metabolic Control, German Cancer Research Center (DKFZ) Heidelberg, 69120 Heidelberg, Germany.

2. Core Facility Tumor Models, DKFZ-ZMBH Alliance, German Cancer Research Center (DKFZ) Heidelberg, 69120 Heidelberg, Germany.

3. Institute of Experimental Genetics, Helmholtz Center Munich, 85764 Neuherberg, Germany.

4. Institute of Clinical Pharmacology, Johann Wolfgang Goethe-University, 60590 Frankfurt, Germany.

5. Department of Animal Physiology, Philipps University Marburg, 35043 Marburg, Germany.

6. Center for Integrative Genomics, National Research Center Frontiers in Genetics, University of Lausanne, 1015 Lausanne, Switzerland.

7. Molecular Nutritional Medicine, Else-Kröner Fresenius Center, Technische Universität München, 85350 Freising-Weihenstephan, Germany.

Abstract

Fat-Burning Fat In mammals, fat exists in two forms—the well-known white adipose tissue (WAT), which stores energy and is associated with obesity, and the lesser-known brown adipose tissue (BAT), which burns energy to generate heat. BAT's role in human physiology was once thought to be restricted to newborns, but the recent discovery that adults also harbor functional BAT has re-ignited interest in the factors regulating BAT development and their potential as targets for anti-obesity therapies. Vegiopoulos et al. (p. 1158 , published online 6 May; see the Perspective Ishibashi and Seale ) now show that cyclooxygenase-2 (COX-2), an enzyme critical to prostaglandin synthesis, triggers fat progenitor cells in mice to differentiate into BAT rather than WAT. Mice overexpressing COX-2 displayed increased energy expenditure and were protected from diet-induced obesity.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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