Endocrinology · 1994 · 111 citations · 35 references
NutritionFetal MedicineFeto-placental Amino AcidInsulin SignalingFetal MetabolismEmbryologyPublic HealthPlacental DevelopmentAnimal PhysiologyGrowth HormoneAnimal NutritionNutrient TransferMaternal HealthDevelopmental EndocrinologyEndocrinologyFetal SheepPlacental FunctionDevelopmental BiologyAnimal SciencePhysiologyCarbohydrate MetabolismAlters Feto-placental ProteinMetabolismMedicine
IGF‑1 is an anabolic hormone that may regulate fetal growth by mediating responses to nutrient supply. The study aimed to determine IGF‑1’s effects on fetal metabolism in vivo. Fetal sheep received a continuous infusion of 50 µg h⁻¹ kg⁻¹ IGF‑1 via chronic catheterization. IGF‑1 infusion lowered fetal and maternal amino‑nitrogen and glucose levels, reduced fetal urea production and placental lactate output, without altering blood flows or transfer, indicating anabolic effects on feto‑placental protein and carbohydrate metabolism.
Insulin-like growth factor 1 (IGF-1) is an anabolic hormone in postnatal life and may be an important endocrine regulator of fetal growth. However, its effects on fetal metabolism in vivo have not previously been determined. We studied the effect of 50 micrograms/h.kg IGF-1 infusion in 12 chronically catheterized fetal sheep. Fetal blood amino nitrogen concentrations fell 10% and maternal 7%, consistent with a rise in feto-placental amino acid uptake. Fetal amino acid oxidation, measured by fetal urea production fell by 30% (44.4 +/- 10.5 to 30.9 +/- 8.0 mumol/min). Fetal and maternal blood glucose concentrations both fell by 0.1 mM, consistent with increased feto-placental glucose uptake. Placental lactate production fell 30% (114 +/- 15 to 78 +/- 11 mumol/min), as did fetal and uterine lactate uptake. There was no change in umbilical or uterine blood flows, nor in placental transfer by simple or facilitated diffusion. We conclude that IGF-1 has anabolic effects on feto-placental protein and carbohydrate metabolism. Circulating IGF-1 may in part mediate the regulation of fetal growth in response to fetal nutrient supply.
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Ralph Jacob, Eugene J. Barrett, G. Plewe et al. · Journal of Clinical Investigation · 1989 · 294 citations · Full text