444 Jr. Platform Speaker: The effects of late gestation hypoxia on fetal metabolism. (7th December 2018)

• Record Type: Journal Article
• Authors: Jones, A; Wesolowski, S
• Is Part Of: Journal of animal science. Volume 96(2018)Supplement 3
• Page Start: 231
• Page End: 231
• Publication Date: 2018-12-07
• Subjects: fetal -- gestation; Livestock -- Periodicals; Livestock; Electronic journals; Periodicals; 636.005
• DOI: 10.1093/jas/sky404.502
• Languages: English
• ISSNs: 0021-8812

Abstract

Abstract: Fetal hypoxia is a component of placental insufficiency, which can be induced by heat stress during gestation, increasing litter size, or improper placental vascularity. Placental insufficiency produces intrauterine growth restricted (IUGR) fetuses that exhibit reduced BW, reduced muscularity, and metabolic disturbances. The IUGR fetal sheep demonstrates premature activation of hepatic gluconeogenic gene expression, phosphoenolpyruvate carboxykinase 1 (PCK1) and glucose 6 phosphatase (G6PC). The IUGR fetal sheep also has increased hepatic pyruvate dehydrogenase kinase 4 expression, indicative of reduced glucose oxidation. Importantly, these changes in fetal hepatic metabolism are inversely correlated with fetal oxygenation status. Our objective is to delineate the role of hypoxia on fetal metabolism. We hypothesized that hypoxia would alter fetal whole-body and hepatic metabolism. To investigate this, maternal N2 gas insufflation during late gestation is used to chronically reduce fetal arterial pO2 by 20%. After 9 days of hypoxia, fetal hepatic PCK1 and G6PC were increased. Fetal arterial pCO2 was reduced and arterial lactate concentrations were increased by hypoxia, indicative of increased anearobic metabolism. Fetuses also demonstrated reduced insulin and increased norepinephrine arterial concentrations. Together, these data demonstrate that hypoxia is a key exposure causing fetal metabolic adaptations to in utero insults, and may act synergistically through endocrine changes. Further research is necessary to investigate how the uteroplacental unit may contribute to the fetal metabolic adaptations observed during hypoxia. Understanding these effects of late gestation hypoxia on fetal metabolism is necessary because persistent changes in metabolism may compromise body composition and growth efficiency of these offspring postnatally.