Ovarian function and obesity: Pcos, menopause

Ovarian function and energy metabolism are tightly connected and reciprocally regulated to enable reproduction in food-scarce environment. Reproductive disorders can lead to metabolic disorders and obesity both of which may in turn induce alterations of the menstrual cycle and fertility. A growing body of research documents the effects of endocrine-disrupting chemicals on the differentiation of adipocytes and the central nervous system circuits that control food intake and energy expenditure, as well as influence on reproduction and insulin secretion. Insulin resistance is related to abdominal obesity, and in women, it is often inextricably linked with ovarian dysfunctions, leading to clinical manifestations across the entire female reproductive life. Specifically, obesity in women manifests, as early menarche, subfertility, polycystic ovary syndrome, symptomatic menopause, and increased risk of breast cancer. Overall, obese women with superimposed reproductive complications including PCOS may be considered to be at high risk for further progression to metabolic syndrome, type 2 diabetes mellitus, and potentially cardiovascular diseases. These patients can then be targeted for early screening, lifestyle optimization, and the prevention of the subsequent metabolic derangement. Considering the reciprocal interactions between pathways that control fertility and energy metabolism and the key roles of molecules such as estrogens and IGF-1 in these pathways, it is possible to consider changing the current therapeutic strategies—amelioration of metabolic disorders, for example, might become an important goal of hormone replacement therapy (HRT) in menopausal obese women.