Ragnheidur Valdimarsdottir

Polycystic ovary syndrome (PCOS) affects 5-10% of women of reproductive age and is currently the leading cause of anovulatory infertility worldwide. Women suffering from PCOS often exhibit distressing overt symptoms such as hirsutism, alopecia and persistent acne, and additionally, the syndrome is strongly associated with numerous comorbidities, including obesity and insulin resistance, cardiovascular disease, endometrial cancer and depression. Despite the prevalence and obvious clinical relevance of PCOS and androgen excess, the mechanisms that mediate the development and pathophysiology of the chronic disease remain obscure. Recently it was demonstrated by using a mouse model that fetal exposure to excess anti-müllerian hormone (AMH) induces PCOS-like phenotypic traits in the offspring. This study will follow up on this finding by evaluating how exposure during fetal life to the two predominant hormones involved in PCOS, i.e. AMH and testosterone, influence offspring birthweight and growth trajectories. With more knowledge about hormonal exposure in relation to these outcomes, we will increase the possibility of early identification of individuals that run an increased risk of childhood obesity, and PCOS later in life.