Abstract
BackgroundA low oxygen supply to the fetus causes intrauterine growth restriction and can affect gonadal development of the offspring, having a potential impact on fertility. We investigated histology and gene expression in the postnatal rat ovary after fetal hypoxia induced by uterine artery ligation.MethodsSprague-Dawley rats underwent uterine artery ligation at day 19 of gestation. Offspring were sacrificed at 5, 20 and 40 days post-partum. Follicles were counted and classified in hematoxylin-eosin stained sections. Gene expression of 90 genes was analyzed by TaqMan® Low Density Array.ResultsA significantly lower number of total and primordial follicles was detected in 20 days post-partum intrauterine growth restricted animals. Follicle density was not different at 40 days post-partum, suggesting that compensatory mechanisms occurred during the pre-pubertal window. Uterine artery ligation modified the expression of 24 genes involved in different cellular functions, among which proliferation, apoptosis and metabolism.ConclusionOvarian follicle pool was affected by fetal hypoxia in early life, but this effect did not persist in puberty. Genes involved in cellular processes were affected at all ages, potentially implying long-term genetic alterations. Further analyses are needed to elucidate later effects of fetal hypoxia on ovarian function and fertility.
Highlights
A low oxygen supply to the fetus causes intrauterine growth restriction and can affect gonadal development of the offspring, having a potential impact on fertility
Mean birth weight (BW) in intrauterine growth restriction (IUGR) rats was still significantly reduced at 5 dpp compared to sham rats but caught up by 20
Fetal life is the first fundamental window of susceptibility to pathogenic noxae for the individual. Events occurring during this period have been associated with gene reprogramming and modification of organ functions that can persist throughout the entire lifespan
Summary
A low oxygen supply to the fetus causes intrauterine growth restriction and can affect gonadal development of the offspring, having a potential impact on fertility. In the early ‘90s David Barker and colleagues published several epidemiological studies correlating birth weight with metabolic risk and rates of death for cardiovascular diseases in adulthood [1,2,3,4,5,6]. These observations gave origin to the theory that adult diseases’ predisposition originates in fetal life, as a consequence of a suboptimal intrauterine environment leading to poor growth of the fetus [4]. Girls born SGA have higher FSH levels during infancy [12, 13], an earlier onset of puberty [14, 15] and a lower age at menarche [15,16,17] than those with a birth weight appropriate for gestational age (AGA)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
