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17b-estradiol increases Slc2a4/GLUT4 expression in 3T3-L1 adipocytes via ESR1.

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Author(s):
Raquel Saldanha Campello
Total Authors: 1
Document type: Doctoral Thesis
Press: São Paulo.
Institution: Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI)
Defense date:
Examining board members:
Ubiratan Fabres Machado; Rodrigo Palazzo de Almeida Barros; Maria de Fatima Magalhães Lazari; Fernanda Ortis; Patricia Monteiro Seraphim
Advisor: Ubiratan Fabres Machado
Abstract

GLUT4 (gene Slc2<font face=\"symbol\">a4) is responsible by insulin-induced glucose uptake and alterations in its expression are related to insulin resistance (IR). Variability in estradiol levels (E2) is related with IR and lower glucose transporter expression and this mechanism can be mediated by transcriptional factor NF<font face=\"symbol\">k-B, which is an Slc2<font face=\"symbol\">a4 repressor. Our aim was to evaluate in 3T3-L1 adipocytes the role of E2 in Slc2<font face=\"symbol\">a4/GLUT4 expression, NF<font face=\"symbol\">k-B binding activity and glucose uptake as well as the ESR1 (estrogen receptor 1) role in this regulation. For this, 3T3-L1 cells were treated for 1 day with E2 and PPT (ESR1-agonist). PPT enhanced Slc2<font face=\"symbol\">a4/GLUT4 expression in the absence or presence of E2 as well as the glucose uptake and decreased NF<font face=\"symbol\">k-B binding activity. Our results show that E2 increases Slc2<font face=\"symbol\">a4/GLUT4 expression via ESR1 and this effect is partially mediated by NF<font face=\"symbol\">k-B, and allow parallel changes in glucose uptake. (AU)

FAPESP's process: 09/02217-1 - GLUT4 gene regulation by estrogen: role of receptors ER alfa and ER beta
Grantee:Raquel Saldanha Campello
Support Opportunities: Scholarships in Brazil - Doctorate