First, FST can disrupt follicle-stimulating hormone secretion by inhibiting activin activity, which hampers follicular development and increases the production of ovarian androgens, both key pathological elements of PCOS.[32] Furthermore, an inverse relationship exists between FST levels and adiponectin, a protein that enhances the body’s response to insulin,[37] and a positive relationship with blood insulin levels and the accumulation of fat in abnormal locations, specifically in the liver. Here, ADIPOQ is linked to polycystic ovary syndrome.