Abstract
Uteroplacental insufficiency (UPI) reduces uterine blood flow leading to low birth weight offspring with programmed adult bone deficits. We investigated the effects of UPI on F1 maternal bone in pregnancy and if deficits are passed to F2 using embryo‐transfer (ET).UPI was induced by bilateral uterine vessel ligation (Restricted, R; Control, C) in rats. One cohort of pregnant F1 C and F1 R rats was culled on embryonic day (E) 20. ET was performed on E1 in a cohort of F1 females, with F2 embryos gestated in Control (C‐in‐C, R‐in‐C) or Restricted (C‐in‐R, R‐in‐R) mothers. Non‐ET offspring were also generated. Growth and pQCT femur analysis was performed.R F1 females were born 10% lighter than C with shorter femurs, lower bone content, density and strength. These differences were absent in pregnancy. F2 non‐ET offspring were born of normal weight and underwent slowed and accelerated growth without transmission of bone deficits. Day 35 male R‐in‐C and R‐in‐R were heavier with longer femurs, increased bone content and strength compared to C‐in‐C/R. Male R embryo groups had accelerated then slowed growth with increased cortical content at 6 months. Restricted ET females did not develop bone deficits.Deficits observed in non‐pregnant F1 R females were absent during pregnancy, indicating restoration of normal skeletal adaptations. Bone deficits are not passed on from a growth restricted mother to her offspring.
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