Polycystic ovary syndrome (pcos) is a complex endocrine disorder affecting 5–10% of women of reproductive age. it has been inferred that pcos can be a familiar genetic syndrome resulted by a combination of genetic and environmental factors. pcos may increase the risk for infertility, dyslipidaemia, cardiovascular disease and endometrial cancer.
A comparative studies performed with women diagnosed as pcos and 30 age and bmi matched healthy women as controls was conducted. fasting blood samples were drawn to measure serum leptin, insulin, fsh, lh, progesterone and testosterone. bmi was also calculated. interpretation of data was done using spss .t‑test was used to compare numerical variables, and the value of p < 0.05 was taken as significant.
Studies show that, the genetic basis of pcos is unknown; not only genes involved in steroid hormone biosynthesis have been studied, but also genes associated with the regulation of insulin secretion and action since hyperinsulinaemia is a characteristic of pcos, because ovarian cells of women with pcos display a higher responsiveness for insulin stimulated androgen synthesis in vitro. leptin acts as permissive signal to maintain normal reproductive function. human obesity is normally associated with hyperleptinemia. increasing obesity is positively correlated to the numbers of anovulatory cycles, and high leptin levels directly inhibit ovarian steroidogenesis, leading to ineffective follicular maturation.
There is a link between elevated serum leptin and insulin levels to obesity in pcos suggesting that most probably they are responsible for the complicated picture of pcos in obese patients.