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Doctoral Thesis
DOI
10.11606/T.42.2012.tde-17042013-101853
Document
Author
Full name
Raquel Saldanha Campello
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2012
Supervisor
Committee
Machado, Ubiratan Fabres (President)
Barros, Rodrigo Palazzo de Almeida
Lazari, Maria de Fatima Magalhães
Ortis, Fernanda
Seraphim, Patricia Monteiro
Title in Portuguese
17b-estradiol aumenta a expressão de Slc2a4/GLUT4 em adipócitos 3T3-L1 via ESR1.
Keywords in Portuguese
Endocrinologia
Estradiol
Glicose
Resistência
Abstract in Portuguese
O GLUT4 (gene Slc2a4) é responsável pela captação de glicose sob estímulo insulínico, e alterações na sua expressão se relacionam à resistência à insulina (RI). Variações na concentração de estradiol (E2) estão relacionadas a RI e menor expressão deste transportador, mecanismo que pode ser mediado pelo fator transcricional NFk-B, um repressor de Slc2a4. Avaliou-se em células 3T3-L1 a regulação da expressão de Slc2a4/GLUT4, a atividade de ligação de NFk-B e a captação de glicose pelo E2 e o papel de ESR1 (isoforma 1 do receptor de E2) nesta regulação. Tratou-se as células por 1 dia com E2 e PPT (agonista de ESR1). O PPT aumentou a expressão de Slc2a4/GLUT4 na ausência ou presença de E2 bem como a captação de glicose e diminuiu a atividade de ligação de NFk-B. Os resultados apresentados demonstram que o E2, atuando via ESR1 aumenta a expressão de Slc2a4/GLUT4, efeitos estes parcialmente mediados por NFk-B, resultando em alteração na captação de glicose.
Title in English
17b-estradiol increases Slc2a4/GLUT4 expression in 3T3-L1 adipocytes via ESR1.
Keywords in English
Endocrinology
Estradiol
Glucose
Resistance
Abstract in English
GLUT4 (gene Slc2a4) 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 NFk-B, which is an Slc2a4 repressor. Our aim was to evaluate in 3T3-L1 adipocytes the role of E2 in Slc2a4/GLUT4 expression, NFk-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 Slc2a4/GLUT4 expression in the absence or presence of E2 as well as the glucose uptake and decreased NFk-B binding activity. Our results show that E2 increases Slc2a4/GLUT4 expression via ESR1 and this effect is partially mediated by NFk-B, and allow parallel changes in glucose uptake.
 
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Publishing Date
2013-05-22
 
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