Hey Mercedes. It depends on the Estrogen receptor you are agonizing. Low ER2 does not effect GLUT 4 expression in muscle cells, though ER1 does. Here is a study a fellow rep posted
Abstract
Estrogen is known to influence glucose homeostasis with dominant effects in the liver, but the role of estrogen receptors in muscle glucose metabolism is unknown. In the present study, we investigated the expression of the two estrogen receptors, ER1 and ER2, and their influence on regulation of the glucose transporter, GLUT4, and its associated structural protein, caveolin-1, in mouse gastrocnemius muscle. Immunohistochemical analysis revealed that ER1 and ER2 are coexpressed in the nuclei of most muscle cells, and that their levels were not affected by absence of estradiol [in aromatase-knockout (ArKO) mice]. GLUT4 expression on the muscle cell membrane was not affected by loss of ER2 but was extremely reduced in ER1-/- mice and elevated in ArKO mice. RT-PCR confirmed a parallel reduction in GLUT4 mRNA levels in ER1-/- mice. Upon treatment of ArKO mice with the ER2 agonist 2,3-bis(4-hydroxyphenyl)propionitrile, GLUT4 expression was reduced. By immunofluorescence and Western blotting, caveolin-1 expression was higher in ArKO mice and lower in ER2-/- and ER1-/- mice than in WT littermates. GLUT4 and caveolin-1 were colocalized in WT and ArKO mice but not in ER2-/- and ER1-/- mice. These results reveal that ER1 is a positive regulator of GLUT4 expression, whereas ER2 has a suppressive role. Both ER2 and ER1 are necessary for optimal caveolin-1 expression. Taken together, these results indicate that colocalization of caveolin-1 and GLUT4 is not an absolute requirement for muscle glucose metabolism but that reduction in GLUT4 could be contributing to the insulin resistance observed in ER1-/- mice.
