Sustained obesity reduces litter size by decreasing proteins regulating folliculogenesis and ovulation in rats - A cafeteria diet model.

Global rise in obesity at early age due to overconsumption of energy-dense food is the major health problem which increases the exposure to obesity over longer duration. Recently we reported that the severity of ovarian dysfunction depends on the duration of obesity. In the present study, we examined the consequences of sustained obesity on reproductive outcome and the underlying mechanism. Sprague Dawley female rats (21 days old) were fed ad libitum with a standard diet (control group) and a cafeteria diet (Obese group) for 32 weeks. We observed hypoprolactinemia, sub-fecundity, sub-fertility, delayed conception and macrosomic pups of reduced litter size in sustained obese rats. The observed decrease in the number of ovarian follicles (primordial, primary, secondary and antral follicles) and corpus luteum indicates impairment in folliculogenesis and ovulation. This impairment might be due to decreased level of ovarian proteins (PRLR, AR, GDF-9, OCT-4, COX-2, PPARγ, ER and PR subtypes) in obese rats. We conclude that sustained obesity impaired folliculogenesis and ovulation thereby increased the severity of reproductive deficits.