ArticleAmerican journal of physiology. Endocrinology and metabolism2015
Coordinated changes in hepatic amino acid metabolism and endocrine signals support hepatic glucose production during fetal hypoglycemia.
Article in American journal of physiology. Endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Experimental chronic fetal hyperglucagonemia stimulates hepatic pathways for amino acid catabolism and gluconeogenesis.The Journal of endocrinology · 2026Article
- Hypoxic pregnancy promotes fibrosis and increases stress metabolites in the ovine fetal liver.The Journal of physiology · 2025Article
- Increased hepatic glucose production with lower oxidative metabolism in the growth-restricted fetus.JCI insight · 2024Article
- Adaptive responses in uteroplacental metabolism and fetoplacental nutrient shuttling and sensing during placental insufficiency.American journal of physiology. Endocrinology and metabolism · 2023Article
- Article
- In vitro- and in vivo-produced male dairy calves show molecular differences in the hepatic and muscular energy regulation†.Biology of reproduction · 2022Article
- Metabolic Consequences of Glucocorticoid Exposure before Birth.Nutrients · 2022Review
- Tissue-specific responses that constrain glucose oxidation and increase lactate production with the severity of hypoxemia in fetal sheep.American journal of physiology. Endocrinology and metabolism · 2022Article
- Uteroplacental nutrient flux and evidence for metabolic reprogramming during sustained hypoxemia.Physiological reports · 2021Article
- Regulation of maternal-fetal metabolic communication.Cellular and molecular life sciences : CMLS · 2021Review
- Dimming the Powerhouse: Mitochondrial Dysfunction in the Liver and Skeletal Muscle of Intrauterine Growth Restricted Fetuses.Frontiers in endocrinology · 2021Review
- Effects of chronic hyperinsulinemia on metabolic pathways and insulin signaling in the fetal liver.American journal of physiology. Endocrinology and metabolism · 2020Article
- Sustained hypoxemia in late gestation potentiates hepatic gluconeogenic gene expression but does not activate glucose production in the ovine fetus.American journal of physiology. Endocrinology and metabolism · 2019Article
- Differential effects of intrauterine growth restriction and a hypersinsulinemic-isoglycemic clamp on metabolic pathways and insulin action in the fetal liver.American journal of physiology. Regulatory, integrative and comparative physiology · 2019Article
- A double-hit pre-eclampsia model results in sex-specific growth restriction patterns.Disease models & mechanisms · 2019Article
- Evidence for liver energy metabolism programming in offspring subjected to intrauterine undernutrition during midgestation.Nutrition & metabolism · 2019Article
- Guinea pig models for translation of the developmental origins of health and disease hypothesis into the clinic.The Journal of physiology · 2018Article
- Ovine uteroplacental and fetal metabolism during and after fetal cortisol overexposure in late gestation.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Exogenous amino acids suppress glucose oxidation and potentiate hepatic glucose production in late gestation fetal sheep.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Role of placental insufficiency and intrauterine growth restriction on the activation of fetal hepatic glucose production.Molecular and cellular endocrinology · 2016Article
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6 authors.
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Abstract
Reduced fetal glucose supply, induced experimentally or as a result of placental insufficiency, produces an early activation of fetal glucose production. The mechanisms and substrates used to fuel this increased glucose production rate remain unknown. We hypothesized that in response to hypoglycemia, induced experimentally with maternal insulin infusion, the fetal liver would increase uptake of lactate and amino acids (AA), which would combine with hormonal signals to support hepatic glucose production. To test this hypothesis, metabolic studies were done in six late gestation fetal sheep to measure hepatic glucose and substrate flux before (basal) and after [days (d)1 and 4] the start of hypoglycemia. Maternal and fetal glucose concentrations decreased by 50% on d1 and d4 (P < 0.05). The liver transitioned from net glucose uptake (basal, 5.1 ± 1.5 μmol/min) to output by d4 (2.8 ± 1.4 μmol/min; P < 0.05 vs. basal). The [U-¹³C]glucose tracer molar percent excess ratio across the liver decreased over the same period (basal: 0.98 ± 0.01, vs. d4: 0.89 ± 0.01, P < 0.05). Total hepatic AA uptake, but not lactate or pyruvate uptake, increased by threefold on d1 (P < 0.05) and remained elevated throughout the study. This AA uptake was driven largely by decreased glutamate output and increased glycine uptake. Fetal plasma concentrations of insulin were 50% lower, while cortisol and glucagon concentrations increased 56 and 86% during hypoglycemia (P < 0.05 for basal vs. d4). Thus increased hepatic AA uptake, rather than pyruvate or lactate uptake, and decreased fetal plasma insulin and increased cortisol and glucagon concentrations occur simultaneously with increased fetal hepatic glucose output in response to fetal hypoglycemia.
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