Reproduction Abstracts

Introduction: The CDC reports that roughly one-third of USA adults suffer from metabolic syndrome. Amongst other health complications, metabolic syndrome is associated with subfertility and complications later in pregnancy. Successful implantation and pregnancy require the priming of both embryo and uterus during a short window of time called the ‘window of implantation’. At this time, hormones stimulate uterine stromal fibroblasts to differentiate into specialized secreting cells in a process termed endometrial decidualization.

Materials and methods: Here, we hypothesized that metabolic syndrome, induced by 6 weeks of high fructose (HFrD) feeding in mice, would impair endometrial decidualization leading to subfertility and altered fetal growth. To study endometrial decidualization, induced deciduomas were used. Additionally, embryos were cultured in 4 mM D-fructose or L-glucose (two-cell to blastocyst) and transferred into normoglycemic dams (CON) to examine possible effects of HFrD on embryonic competence.

Results and discussion: HFrD feeding induced metabolic syndrome, characterized by decreased glucose tolerance, hepatic steatosis, and elevated circulating lipids. Litter size was decreased by 37% and birth weights were significantly reduced in HFrD mice compared with CON. Induced deciduoma weights were 50% smaller in HFrD mice. Conversely, implantation rates were similar between D-fructose (36%) and L-glucose exposed embryos (30%), suggesting that reduced litter size in HFrD mice may be a consequence of impaired uterine receptivity as opposed to altered embryonic competence. However, at E14.5 crown-rump lengths of D-fructose exposed embryos were significantly shorter and their placentas were smaller compared to L-glucose embryos, suggesting that embryonic exposure to HFrD may alter fetal–placental development.