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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Estradiol stimulates adipogenesis and Slc2a4/GLUT4 expression via ESR1-mediated activation of CEBPA

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Author(s):
Fatima, Luciana A. [1] ; Campello, Raquel S. [1] ; Barreto-Andrade, Joao N. [1] ; Passarelli, Marisa [2, 3] ; Santos, Roberta S. [4] ; Clegg, Deborah J. [4] ; Machado, Ubiratan F. [1]
Total Authors: 7
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, Av Prof Lineu Prestes 1524, BR-05508900 Sao Paulo - Brazil
[2] Univ Sao Paulo, Med Sch, Lipids Lab LIM 10, Sao Paulo - Brazil
[3] Univ Nove Nove Julho, Grad Studies Program Med, Sao Paulo - Brazil
[4] Cedars Sinai Med Ctr, Biomed Res Dept, Diabet & Obes Res Div, Los Angeles, CA 90048 - USA
Total Affiliations: 4
Document type: Journal article
Source: Molecular and Cellular Endocrinology; v. 498, DEC 1 2019.
Web of Science Citations: 0
Abstract

The ability of adipose tissue to expand is dependent on adipocyte differentiation and adipose tissue glucose disposal. The CCAAT/enhancer-binding protein alpha (CEBPA) enhances the expression of the Slc2a4 gene and GLUT4 protein, which are markers of adipocyte differentiation/glucose disposal. We hypothesized estradiol (E2) facilitates adipocyte differentiation/glucose disposal by an estrogen receptor 1 (ESR1)-dependent and CEBPA-mediated mechanism. Our results suggest that E2 (10 nM) has a positive effect on 3T3-L1 adipocyte differentiation (days 2-8), lipid accumulation, Slc2a4 and Cebpa mRNA expression, total GLUT4 and nuclear CEBPA contents, and CEBP/Slc2a4-binding activity. Esr1 silencing (similar to 50%) in mature adipocytes abrogates the 24-h E2 effects on nuclear CEBPA content, Slc2a4/GLUT4 expression and GLUT4 translocation to the cell membrane. Thus, E2 stimulates adipocyte differentiation and Slc2a4/GLUT4 expression in an ESR1/CEBPA-mediated pathway. Our data provide mechanistic insight demonstrating E2 participates in adipose-tissue differentiation and glucose transporter expression which ultimately can improve adipose tissue expandability and glycemic control. (AU)

FAPESP's process: 16/15603-0 - Unraveling mechanisms of glycemic control and chronic complications of Diabetes mellitus: contributions to human health
Grantee:Ubiratan Fabres Machado
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 12/24210-1 - REGULATION OF Slc2a4/GLUT4 EXPRESSION BY 17²-ESTRADIOL
Grantee:Raquel Saldanha Campello
Support Opportunities: Scholarships in Brazil - Post-Doctoral