Pregnant growth restricted female rats have bone gains during late gestation which contributes to second generation adolescent and adult offspring having normal bone health

摘要: Abstract Low birth weight, due to uteroplacental insufficiency, results in programmed bone deficits the first generation (F1). These may be passed onto subsequent generations. We characterized effects of being born small on maternal health during pregnancy; and aimed characterize contribution environment germ line F2 offspring from mothers small. Bilateral uterine vessel ligation (or sham) surgery was performed female F0 WKY rats gestational day 18 (term 22 days) induce insufficiency fetal growth restriction. Control Restricted F1 were allocated a non-pregnant or pregnant group. To generate offspring, females either non-embryo embryo transfer groups. Embryo 1, where second (F2) embryos gestated (donor-in-recipient) (Control-in-Control, Restricted-in-Control) (Control-in-Restricted, Restricted-in-Restricted) mother. 10–15% lighter than Controls. had shorter femurs, reduced trabecular cortical mineral contents, density geometry measures determined by peripheral quantitative computed tomography (pQCT) compared Pregnancy restored that present females. male normal while males mother heavier at (Restricted-in-Restricted, Control-in-Restricted). Male groups (Restricted-in-Control accelerated postnatal growth. There no transmission 35 days 6 months offspring. procedure confounding preventing separation outcomes. Deficits absent late gestation, indicating experienced gains bone. beneficial pregnancy adaptations have prevented