The influence of maternal obesity during oocyte development and its putative interaction with nutrient reserves at conception on pregnancy outcome were examined in an adolescent sheep model. Donor ewes were nutritionally managed to achieve contrasting adiposity (control [CD]/obese [ObD]) for 6 weeks prior to superovulation, and inseminated by a non-obese sire. Morulae from 6 CD and 7 ObD were transferred in singleton into adolescent recipients of identical age but differing adiposity, classified as relatively fat or thin, respectively. Thereafter all were overnourished to promote rapid growth/adiposity (2x2 design, 13/14 pregnancies/group). A fifth recipient group of intermediate adiposity received embryos from another 5 CD, were offered a moderate intake to maintain adiposity throughout gestation and acted as controls for normal pregnancy outcome (optimally-treated-control [OTC], 19 pregnancies). Donor obesity did not influence ovulation, fertilization or recovery rates or impact embryo morphology. Gestation length and colostrum yield were unaffected by donor or recipient adiposity and were reduced relative to OTC. Total fetal cotyledon and lamb birth weights were independent of initial donor adiposity but reduced in relatively thin versus relatively fat recipients, and lower than in the OTC group. In spite of high placental efficiency, the incidence of fetal growth-restriction was greatest in the thin recipients. Thus maternal adiposity at conception, but not pre-conception maternal obesity, modestly influences the feto-placental growth trajectory, while comparison with the OTC indicates that high gestational-intakes to promote rapid maternal growth remain the dominant negative influence on pregnancy outcome in young adolescents. These findings inform dietary advice for pregnant adolescent girls.
Wallace, J. M., Milne, J. S., Adam, C. L., & Aitken, R. P. (2017). Impact of donor and recipient adiposity on placental and fetal growth in adolescent sheep. Reproduction, 153(4), 381-394. https://doi.org/10.1530/REP-16-0590