It is well established that insulin resistance (IR) and compensatory hyperinsulinaemia are central aetiological abnormalities in women with PCOS which lead to the overproduction of ovarian and adrenal androgens and an increase in androgen bioavailability through inhibition of sex hormone-binding globulin (SHBG) secretion [10]. Here, SHBG is linked to polycystic ovary syndrome.