PCOS is thought to be produced by an autosomal dominant inheritance pattern, and there is evidence to support this theory in the form of family clustering of instances. The investigations, on the other hand, have been hindered by things like limited sample numbers, statistical mistakes, and diagnostic disparities. Based on the findings, it appears that polycystic ovary syndrome is caused by a fundamental genetic defect in the synthesis of ovarian androgens, which then interacts with environmental conditions or other factors that lead to hyperinsulinemia. The suspected PCOS gene is connected to a region on chromosome 19p13.3, which is located close to the gene for the insulin receptor. Additional molecular genetic techniques offer the potential to provide light on the pathogenesis of polycystic ovary syndrome (PCOS).
Polycystic Ovary Syndrome (PCOS) is a complex trait with an oligogenic basis, with genetic factors playing a role. Environmental contributions are crucial, as there are no universally accepted genes important in PCOS etiology. Two approaches are used to identify a genetic locus: association studies and linkage studies. Genetic abnormalities affect signal transduction, steroid hormones, insulin action, energy homeostasis, and chronic inflammation.