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

Autor(es)

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]

Afiliação do(s) autor(es)

^[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

• Tipo de documento: Artigo Científico
• Fonte: Molecular and Cellular Endocrinology; v. 498, DEC 1 2019.
• Citações Web of Science: 0

Resumo

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)

• Processo FAPESP: 16/15603-0 - Desvendando mecanismos envolvidos no controle glicêmico e nas complicações crônicas do Diabetes mellitus: contribuições à saúde humana
• Beneficiário: Ubiratan Fabres Machado
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 12/24210-1 - REGULAÇÃO DA EXPRESSÃO DE Slc2a4/GLUT4 PELO 17²-ESTRADIOL
• Beneficiário: Raquel Saldanha Campello
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado