Abstract

Obesity is one of the tpks inducing factors in women. It is known that there is a positive correlation between obesity and insulin resistance and hyperinsulinemia. In particular, insulin and IGF 17-al'fa can induce hydroxylase and LG receptor ecpression. Perhaps, it is through this pathogenetic mechanism that hyperinsulinemia can cause the development of TPKS in many cases. After all, pathological conditions such as hyperinsulinemia and insulin resistance increase the LG sensitivity of thecocytes and disrupt its repression by re-negative binding . For this reason, as a result of increased LG secretion in tpks pathogenesis, and as a result of tecocyte hyperplasia and LG indusiratory hypeandrogenemia, the capture of follicles in antral state (non-ovulation) causes specific cystic structures to originate after a certain period of time.