Endocrine Abstracts (2011) 26 P358

Chronic effect of 17[beta] estradiol on GLUT4 expression in 3T3-L1 adipocytes

R S Campello, A C Poletto, D T Furuya, R C T Mori & U F Machado


Universty of São Paulo, São Paulo, Brazil.


Introduction: Insulin resistance results from a combination of genetic and environmental factors and it may be considered the primary cause of the development of metabolic disorders, such as type 2 diabetes mellitus. It is characterized by a reduced ability of insulin sensitivity tissues to respond to normal levels of the hormone. In these tissues, glucose transport stimulated by insulin occurs through the glucose transporter 4 and alterations in its expression are related to changes in insulin sensitivity. It is known estradiol (E2) modulates insulin sensitivity and previous studies in skeletal muscle revealed it also participates in the GLUT4 regulation. Thus, the aim of this study was to investigate the effect of 17β Estradiol on GLUT4 expression in 3T3-L1 adipocytes.

Methods: 3T3-L1 cells were treated with increasing doses of 17β Estradiol (0, 0.1, 1, 10 and 100 nM), for different periods of time (12, 24 and 48 h). After treatment, GLUT4 protein content was quantified by western blotting and mRNA expression by real time-PCR.

Results: GLUT4 protein content increased significantly (19–56%) after 24 h of E2 treatment, in all of the concentrations analyzed, as compared to control (0 nM). Furthermore, after 48 h of treatment, cells exposed to E2 (0.1 nM) also presented a significantly increase (16%) in GLUT4 protein content, comparing to the other doses. GLUT4 mRNA content increased significantly (20–30%) after 12 h of treatment in intermediate doses (1 and 10 nM), as compared to control (0 nM). However, after 24 or 48 h, no significant difference was observed in GLUT4 mRNA content in any of the doses evaluated.

Conclusion: Results suggested a time and dose dependent E2 effect on GLUT4 expression in 3T3-L1 adipocytes, in addition to a possible post-transcriptional modulation in the presence of the hormone.

Funding: FAPESP 2009/02217-1.

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