Abstract P217: Phenotypic Difference Exist Between Bph/5 Offspring In A Sex-dependent Manner

Abstract

Preeclampsia (PE) is a hypertensive disorder of pregnancy occurring in ~10% of women worldwide. Maternal obesity is a risk factor for PE and the effects on offspring are long-standing with increased incidence of cardiometabolic disease into adulthood. The maternal obesogenic environment may play a role in pregnancy outcomes and offspring in a sex-dependent manner; however, in the context of superimposed PE, it is not completely understood. Obese BPH/5 mice spontaneously exhibit late-gestational hypertension, fetal demise and growth restriction, and excessive gestational weight gain, similar to PE. We hypothesized that phenotypic differences exist between female and male BPH/5 offspring and maternal weight loss in BPH/5 during pregnancy would influence these phenotypic differences. Obese BPH/5 dams were calorie restricted via pair-feeding (PF) to match the food intake of C57 dams for the first 9 days of pregnancy. Offspring were fed an ad libitum (lib) diet until phenotypic analysis. Body weights (BW), visceral peri-gonadal and peri-renal white adipose tissue (WAT), hearts, and livers were recorded in BPH/5 and control C57 age-matched adult females and males born to ad lib fed and PF dams. Values are reported as mean ± standard error of the mean. As previously described, BPH/5 females born to ad lib fed dams are overweight with increased peri-renal and gonadal WAT, cardiomegaly, and hepatomegaly (1308 ±13.3 vs 979.9 ±82.3g in C57, p<0.05). BPH/5 male mice are underweight (23.8±1.6 vs C57: 27.9±1.6g) with increased peri-renal WAT (158± 23 vs C57: 53.25±10.3mg, p<0.05), and cardiomegaly (heart: BW 8.1±0.5 vs C57: 5.7±1.1, p<0.05). Without altering BPH/5 male or female offspring BW, peri-renal adiposity (males: 103.5±13mg, females: 73.2±10.3mg, p<0.05), cardiomegaly (males: 5.74±0.5, females: 6.03±0.4, p<0.05), and female hepatomegaly (1149.8 ±58.1mg, p<0.05) are significantly attenuated in PF BPH/5 dams. To conclude, reduction in the maternal obesogenic environment may play a role in BPH/5 sex-dependent phenotypic differences. Future investigations are necessary to understand the differences observed in BPH/5 male versus female mice into adulthood as well as the transgenerational impact of attenuated maternal obesity in pregnancy.