Estrogen Conversion and Receptors: Difference between revisions

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The main feminizing effects of estrogen depend on sex-hormone receptors being present in cells and hormone molecules being free to bind to them to affect gene expression. Since sex-hormones also regulate receptor expression<ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9934771/</ref>, increasing the amount of receptors or hormone available for binding is thus a desirable goal for feminizing HRT.<ref>https://springerplus.springeropen.com/articles/10.1186/2193-1801-2-214</ref>
The main feminizing effects of estrogen depend on sex-hormone receptors being present in cells and hormone molecules being free to bind to them to affect gene expression. Since sex-hormones also regulate receptor expression<ref>https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9934771/</ref>, increasing the amount of receptors or hormone available for binding is thus a desirable goal for feminizing HRT.<ref>https://springerplus.springeropen.com/articles/10.1186/2193-1801-2-214</ref>



Latest revision as of 04:54, 18 March 2024


The main feminizing effects of estrogen depend on sex-hormone receptors being present in cells and hormone molecules being free to bind to them to affect gene expression. Since sex-hormones also regulate receptor expression[1], increasing the amount of receptors or hormone available for binding is thus a desirable goal for feminizing HRT.[2]

Estradiol has a pathway of being synthesized from testosterone in the body through an enzyme called aromatase which allows for certain levels of testosterone to circulate and still be converted to estrogen.[3]

This conversion of sex-hormones has an important effect on sites such as the breasts, fat, bones and brain which are affected by local synthesis of estradiol acting directly on the tissues[4].[5] [6]