Maternal adiponectin prevents visceral adiposity and adipocyte hypertrophy in prenatal androgenized female mice

Hyperandrogenism is the main characteristic of polycystic ovary syndrome, which affects placental function and fetal growth, leads to reproductive metabolic dysfunction in female offspring. Adiponectin acts on placenta may exert endocrine effects developing fetus. This study aims investigate if maternal and/or adiponectin can prevent prenatal androgenized (PNA) transgenic (APNtg) wild-type dams received dihydrotestosterone/vehicle injections between gestational days 16.5-18.5 induce PNA offspring, were followed for 4 months. Offspring from APNtg smaller than offspring dams, independent genotype. Insulin sensitivity was higher mice compared wild-types insulin correlated with fat mass adipocyte size. increased visceral fat% size while protected against this effect. had adipocytes morphology associated an expression genes regulating adipogenesis (Ppard, Pparg, Cebpa, Cebpb) metabolism (Chrebp Lpl). Anogenital distance all PNA-exposed but there no increase suggesting that overexpression protects In conclusion, elevated levels utero improve sensitivity, reduce body weight gain adult protect PNA-induced adiposity. these data suggest benefit supplementation.