Abstract
BackgroundEmbryonic and fetal exposure to maternal obesity causes several maladaptive morphological and epigenetic changes in exposed offspring. The timing of these events is unclear, but changes can be observed even after a short exposure to maternal obesity around the time of conception. The hypothesis of this work is that maternal obesity influences the ovine preimplantation conceptus early in pregnancy, and this exposure will affect gene expression in embryonic and extraembryonic tissues.ResultsObese and lean ewe groups were established by overfeeding or normal feeding, respectively. Ewes were then bred to genetically similar rams. Conceptuses were collected at day 14 of gestation. Morphological assessments were made, conceptuses were sexed by genomic PCR analysis, and samples underwent RNA-sequencing analysis. While no obvious morphological differences existed between conceptuses, differentially expressed genes (≥ 2-fold; ≥ 0.2 RPKM; ≤ 0.05 FDR) were detected based on maternal obesity exposure (n = 21). Also, differential effects of maternal obesity were noted on each conceptus sex (n = 347). A large portion of differentially expressed genes were associated with embryogenesis and placental development.ConclusionsFindings reveal that the preimplantation ovine conceptus genome responds to maternal obesity in a sex-dependent manner. The sexual dimorphism in response to the maternal environment coupled with changes in placental gene expression may explain aberrations in phenotype observed in offspring derived from obese females.
Highlights
Embryonic and fetal exposure to maternal obesity causes several maladaptive morphological and epigenetic changes in exposed offspring
Conceptus length, conceptus sex ratio and IFNT production were not affected by maternal obesity status or conceptus sex at day14
Localized inflammatory responses are observed in the rat and horse uterus in an obese state, and these responses are probably driven, at least in part, by pro-inflammatory cytokine actions within the endometrium [89, 90]. These and other pro-inflammatory factors likely affect uterine homeostasis in ways that cause conceptuses to respond differently to their uterine environment. These results indicate that the conceptus genome is susceptible to perturbations caused by maternal obesity early in development, even though morphological changes to the conceptus nor alterations in maternal reproductive parameters are detectable
Summary
Embryonic and fetal exposure to maternal obesity causes several maladaptive morphological and epigenetic changes in exposed offspring. The timing of these events is unclear, but changes can be observed even after a short exposure to maternal obesity around the time of conception. Obesity is a prominent cause of various adverse health conditions, including heart disease, stroke, type 2 diabetes, and some cancers in humans and other mammals [1]. The prevalence of these conditions may be one of the leading causes of preventable death among adults. While the effects of maternal obesity are known to have lasting effects in offspring, methods to alleviate these effects are lacking
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