Parental diet-induced obesity leads to retarded early mouse embryo development and altered carbohydrate utilisation by the blastocyst

Maternal obesity results in reproductive complications, whereas the impact of paternal obesity is unclear. In the present study, the effects of parental obesity on preimplantation embryo cell cycle length and carbohydrate utilisation were investigated. Maternal and paternal obesity were assessed independently by deriving zygotes from normal or obese C57BL/6 female mice mated with normal Swiss male mice (maternal obesity), or from normal Swiss female mice mated with normal or obese C57BL/6 male mice (paternal obesity). Zygotes were cultured in vitro and development was then assessed by time-lapse microscopy and metabolism determined using ultramicrofluorescence. Maternal obesity was associated with a significant delay in precompaction cell cycle kinetics from the 1-cell stage. A significant increase in glucose consumption by embryos from obese compared with normal females occurred after compaction, although glycolysis remained unchanged. Similarly, paternal obesity led to significant delays in cell cycle progression during preimplantation embryo development. However, this developmental delay was observed from the second cleavage stage onwards, following embryonic genome activation. Blastocysts from obese males showed disproportionate changes in carbohydrate metabolism, with significantly increased glycolysis. Overall, metabolic changes were not inhibitory to blastocyst formation; however, blastocyst cell numbers were significantly lower when either parent was obese. These data suggest that both maternal and paternal obesity significantly impacts preimplantation embryo physiology.Natalie K. Binder, Megan Mitchell and David K. Gardne

A retrospective study of the pregnancy, delivery and neonatal outcome in overweight versus normal weight women with polycystic ovary syndrome

Study question: Do overweight women with polycystic ovary syndrome (PCOS) have a higher risk of perinatal complications than normal weight women with PCOS? Summary answer: Overweight women with PCOS with an ongoing singleton pregnancy have an increased risk of preterm birth as well as an increased risk of giving birth to a baby with a higher birth weight than normal weight women with PCOS. What is known already: There is evidence that overweight (BMI. 25 kg/ m2) has a negative influence on the prevalence of gestational diabetes mellitus and fetal macrosomia in women with PCOS. Study design, size, duration: We set up a retrospective comparative cohort study of 93 overweight ( BMI = 25 kg/ m2) and 107 normal weight (BMI, 25 kg/ m2) women with PCOS who were scheduled for fertility treatment between January 2000 and December 2009 and achieved a pregnancy as a result of a treatment cycle, or spontaneously before or between treatment cycles. Participants/ materials, setting, methods: All data (patient characteristics, medical information, pregnancy, delivery and neonatal outcome) were retrieved from patient medical files. All pregnancy, delivery and neonatal outcome parameters were adjusted for age and pre-pregnancy smoking behaviour. The neonatal outcome parameters were additionally adjusted for gestational age. Main results and the role of chance: The median BMI in the overweight and normal weight women was, respectively, 30.8 kg/m2 [interquartile quartile range (IQR) 5.8] and 20.9 kg/ m2 (IQR 2.3) (P, 0.001). Baseline characteristics did not differ between groups, except for free testosterone and fasting insulin levels, which were higher, and sex hormone-binding globulin, which was lower, in overweight versus normal weight women ( all P, 0.001). The time-to-pregnancy was significantly higher in the overweight group ( P = 0.01). Multivariate analyses of the ongoing singleton pregnancies showed significantly more preterm births in overweight ( 10/ 61) versus normal weight (2/ 71) women [adjusted odds ratio 0.1, 95% confidence interval ( CI) 0- 0.6, P = 0.01]. The mean birth weight of newborns was significantly higher in overweight ( 3386 + 663 g) than in normal weight (3251+ 528 g) women ( adjusted mean difference 259.4, 95% CI 83.4- 435.4, P = 0.004). Limitations, reason for caution: Our results only represent the pregnancy, delivery and neonatal outcome of ongoing singleton pregnancies. The rather small sample size and observational nature of the study are further limitations. Wider implications of the findings: Our results suggest the importance of pre-pregnancy weight loss in overweight women with PCOS in order to reduce the risk of adverse perinatal outcomes