C/EBPα and the Corepressors CtBP1 and CtBP2 Regulate Repression of Select Visceral White Adipose Genes during Induction of the Brown Phenotype in White Adipocytes by Peroxisome Proliferator-Activated Receptor γ Agonists
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| Published in | Molecular and Cellular Biology Vol. 29; no. 17; pp. 4714 - 4728 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
American Society for Microbiology
01.09.2009
Taylor & Francis American Society for Microbiology (ASM) |
| Online Access | Get full text |
| ISSN | 0270-7306 1098-5549 1098-5549 |
| DOI | 10.1128/MCB.01899-08 |
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| AbstractList | White adipose tissue (WAT) stores energy in the form of triglycerides, whereas brown tissue (BAT) expends energy, primarily by oxidizing lipids. WAT also secretes many cytokines and acute-phase proteins that contribute to insulin resistance in obese subjects. In this study, we have investigated the mechanisms by which activation of peroxisome proliferator-activated receptor γ (PPARγ) with synthetic agonists induces a brown phenotype in white adipocytes in vivo and in vitro. We demonstrate that this phenotypic conversion is characterized by repression of a set of white fat genes (“visceral white”), including the resistin, angiotensinogen, and chemerin genes, in addition to induction of brown-specific genes, such as
Ucp-1
. Importantly, the level of expression of the “visceral white” genes is high in mesenteric and gonadal WAT depots but low in the subcutaneous WAT depot and in BAT. Mutation of critical amino acids within helix 7 of the ligand-binding domain of PPARγ prevents inhibition of visceral white gene expression by the synthetic agonists and therefore shows a direct role for PPARγ in the repression process. Inhibition of the white adipocyte genes also depends on the expression of C/EBPα and the corepressors, carboxy-terminal binding proteins 1 and 2 (CtBP1/2). The data further show that repression of resistin and angiotensinogen expression involves recruitment of CtBP1/2, directed by C/EBPα, to the minimal promoter of the corresponding genes in response to the PPARγ ligand. Developing strategies to enhance the brown phenotype in white adipocytes while reducing secretion of stress-related cytokines from visceral WAT is a means to combat obesity-associated disorders. Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology. For an alternate route to MCB .asm.org, visit: MCB White adipose tissue (WAT) stores energy in the form of triglycerides, whereas brown tissue (BAT) expends energy, primarily by oxidizing lipids. WAT also secretes many cytokines and acute-phase proteins that contribute to insulin resistance in obese subjects. In this study, we have investigated the mechanisms by which activation of peroxisome proliferator-activated receptor γ (PPARγ) with synthetic agonists induces a brown phenotype in white adipocytes in vivo and in vitro. We demonstrate that this phenotypic conversion is characterized by repression of a set of white fat genes ("visceral white"), including the resistin, angiotensinogen, and chemerin genes, in addition to induction of brown-specific genes, such as Ucp-1. Importantly, the level of expression of the "visceral white" genes is high in mesenteric and gonadal WAT depots but low in the subcutaneous WAT depot and in BAT. Mutation of critical amino acids within helix 7 of the ligand-binding domain of PPARγ prevents inhibition of visceral white gene expression by the synthetic agonists and therefore shows a direct role for PPARγ in the repression process. Inhibition of the white adipocyte genes also depends on the expression of C/EBPα and the corepressors, carboxy-terminal binding proteins 1 and 2 (CtBP1/2). The data further show that repression of resistin and angiotensinogen expression involves recruitment of CtBP1/2, directed by C/EBPα, to the minimal promoter of the corresponding genes in response to the PPARγ ligand. Developing strategies to enhance the brown phenotype in white adipocytes while reducing secretion of stress-related cytokines from visceral WAT is a means to combat obesity-associated disorders. |
| Author | Li Qiang Sidney B. Peres Cecile Vernochet Stephen R. Farmer Meghan E. McDonald Hong Wang Kathryn E. Davis Philipp E. Scherer |
| AuthorAffiliation | Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 02118, 1 Touchstone Diabetes Center, Departments of Internal Medicine and Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas 2 |
| AuthorAffiliation_xml | – name: Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 02118, 1 Touchstone Diabetes Center, Departments of Internal Medicine and Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas 2 |
| Author_xml | – sequence: 1 givenname: Cecile surname: Vernochet fullname: Vernochet, Cecile organization: Department of Biochemistry, Boston University School of Medicine – sequence: 2 givenname: Sidney B. surname: Peres fullname: Peres, Sidney B. organization: Department of Biochemistry, Boston University School of Medicine – sequence: 3 givenname: Kathryn E. surname: Davis fullname: Davis, Kathryn E. organization: Touchstone Diabetes Center, Departments of Internal Medicine and Cell Biology, University of Texas Southwestern Medical Center – sequence: 4 givenname: Meghan E. surname: McDonald fullname: McDonald, Meghan E. organization: Department of Biochemistry, Boston University School of Medicine – sequence: 5 givenname: Li surname: Qiang fullname: Qiang, Li organization: Department of Biochemistry, Boston University School of Medicine – sequence: 6 givenname: Hong surname: Wang fullname: Wang, Hong organization: Department of Biochemistry, Boston University School of Medicine – sequence: 7 givenname: Philipp E. surname: Scherer fullname: Scherer, Philipp E. organization: Touchstone Diabetes Center, Departments of Internal Medicine and Cell Biology, University of Texas Southwestern Medical Center – sequence: 8 givenname: Stephen R. surname: Farmer fullname: Farmer, Stephen R. email: farmer@biochem.bumc.bu.edu organization: Department of Biochemistry, Boston University School of Medicine |
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| Notes | Corresponding author. Mailing address: Department of Biochemistry, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118. Phone: (617) 638-4186. Fax: (617) 638-5339. E-mail: farmer@biochem.bumc.bu.edu |
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Mendeley... White adipose tissue (WAT) stores energy in the form of triglycerides, whereas brown tissue (BAT) expends energy, primarily by oxidizing lipids. WAT also... |
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| Title | C/EBPα and the Corepressors CtBP1 and CtBP2 Regulate Repression of Select Visceral White Adipose Genes during Induction of the Brown Phenotype in White Adipocytes by Peroxisome Proliferator-Activated Receptor γ Agonists |
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