Evidences are there regarding the insulin stimulation of ovarian p450 aromatase expression and activity in vitro. Excess insulin and ovarian production of excess androgens are the cardinal feature of PCOS. Why those excess androgens are not being able to be converted into E2.
Dear Debabrata,
in my opinion it may be due to limited aromatase capacity.
Best regards
Pavel
Dear Debabrata,
I have just the same point of view as Pavel. You may consider this: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4392749/
"Ovarian aromatase activity was decreased in PCOS patients which was independent of BMI".
Kindly regards,
Maksim.
dear Debabrata,
I also agree with my colleagues . In PCOS the activity of aromatase is reduced . How do you know its activity is regulated by FSH . The FSH to work in ovarian level needs a second messenger myoinositolo employee . Because of hyperinsulinemia ( the ovary is never insulinoresistent ) myoinositol is converted into Dchiroinositolo . It follows that the ovary will inpoverito of MYO and will no longer be able to respond to FSH . Hence the anovulation and EPR As for your question , a lower aromatase activity with a reduction in circulating estrogen .
BR
Vittorio
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