Intending parents are now heavier and older than ever before, and we are only just beginning to understand that these physiological changes have long term impacts on the health of their offspring. Our research is focused on elucidating how somatic cells in the ovary nurture the oocyte and endow it with the essential components to form an embryo, and how obesity changes these biological mechanisms. We have discovered, using mouse models, that obesity causes ovarian fibrosis, a state of inflammation and excess collagen, that impairs oocyte release. We also found that obesity impacts the granulosa cells that directly surround the oocyte, specifically mitochondrial respiration is reduced but not glycolysis. Analysis of granulosa cells of women attending a fertility clinic showed similar metabolic changes associated with increasing BMI. Further, we are identifying the molecular changes that occur in oocytes in response to obesity. Remarkably in each these ovarian cell types, the effects of obesity are similar to the effects of aging, raising the alarm that obesity in women causes accelerated reproductive aging. Importantly, we are also focused on developing therapies that can mitigate the effects of obesity on ovarian function, and are generating preclinical data to bring these into clinical use in reproductive medicine.