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Abstract
ObjectiveThe importance of the placenta in mediating the pre- and post-natal consequences of fetal growth restriction has been increasingly recognized. However, the influence of placental sexual dimorphism on driving these outcomes has received little attention. The purpose of this study was to characterize how sex contributes to the relationship between placental metabolism and fetal programming utilizing a novel rodent model of growth restriction. MethodsFetal growth restriction was induced by maternal inhalation of 0.8 ppm ozone (4 h/day) during implantation receptivity (gestation days [GDs] 5 and 6) in Long-Evans rats. Control rats were exposed to filtered air. At GD 21, placental and fetal tissues were obtained for metabolic and genomic assessments. ResultsGrowth-restricted male placentae exhibited increased mitochondrial biogenesis, increased oxygen consumption, and reduced nutrient storage. Male growth-restricted fetuses also had evidence of reduced adiposity and downregulation of hepatic metabolic signaling. In contrast, placentae from growth-restricted females had elevated markers of autophagy accompanied by an observed protection against hepatic metabolic perturbations. Despite this, growth restriction in females induced a greater number of hypothalamic gene and pathway alterations compared to growth-restricted males. ConclusionsIncreases in mitochondrial metabolism in growth-restricted male placentae likely initiates a sequela of adaptations that promote poor nutrient availability and adiposity. Divergently, the female placenta expresses protective mechanisms that may serve to increase nutrient availability to support fetal metabolic development. Collectively, this work emphasizes the importance of sex in mediating alterations in placental metabolism and fetal programming.
Highlights
Intrauterine growth restriction (IUGR) is a prevalent developmental condition that affects upward of 11% of pregnancies in the US [1] and 24% of births in developing countries [2]
We hypothesized that placental sex is a significant contributing factor to the near-term outcomes observed in our model of ozone-induced IUGR, changes that are consistent with differential cardiometabolic disease risk
We focused on alterations in placental mitochondrial bioenergetics due to the important roles that mitochondria play in nutrient and oxygen utilization
Summary
Intrauterine growth restriction (IUGR) is a prevalent developmental condition that affects upward of 11% of pregnancies in the US [1] and 24% of births in developing countries [2]. Defined as a birth weight below the tenth percentile for gestational age, IUGR is a significant cause of both pre- and perinatal mortality [5]. While the rates of IUGR are higher overall in female neonates [8], the risk of perinatal mortality is higher in males [9]. This propensity toward greater complications in males extends to childhood and adulthood, in the components of metabolic syndrome [10]. The most well-studied is hypertension, with restricted growth in utero more closely associated with increased blood pressure in males
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