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Fetal insulin and growth hormone metabolism in the subhuman primate.

Abstract

The concentrations of plasma glucose, insulin, growth hormone, and immunoreactive growth hormone-like substance in subhuman primate fetal and maternal plasma were examined after the intravascular administration of glucose, arginine, or tolbutamide to the fetus. Cannulation of interplacental vessels permitted studies on the fetus in utero without disruption of fetal-placental-maternal anatomic integrity. Single glucose injections, glucose infusions, and arginine infusions into the fetus did not alter fetal plasma insulin concentrations. In contrast, tolbutamide injections elicited an immediate 3-4-fold increase in fetal plasma insulin concentrations. A bidirectional placental transfer of insulin was demonstrated with the use of simultaneously injected insulin-(125)I to the mother and insulin-(131)I to the fetus. Simian fetal plasma contained a substance which cross-reacted with immunologic identity to human growth hormone. In contrast, simian maternal plasma and amniotic fluid reacted with immunologic nonidentity to human growth hormone. Although glucose administration to the fetus did not suppress nor did arginine infusion consistently augment fetal plasma growth hormone levels, the latter were observed to vary in individual experiments. The plasma responses to the same stimuli in the neonate were also examined. In contrast to the fetal experiments, glucose injection in the neonate elicited a delayed rise in the concentration of plasma insulin. Similar to the fetus, the plasma concentration of insulin increased after tolbutamide injection and did not change in response to arginine infusion. The initial concentrations of neonatal plasma growth hormone were significantly lower when contrasted with the initial fetal plasma levels. There was no difference in the responsiveness of the fetal and neonatal growth hormone-releasing mechanisms when challenged by glucose or arginine infusion. The data indicate that the fetal plasma concentration of growth hormone is labile, that fetal growth hormone metabolism may differ from that in the neonate, and that pancreatic islet cell responsiveness rapidly changes after delivery.

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    MeSH

    Animals
    Arginine
    Blood Glucose
    Female
    Glucose
    Growth Hormone
    Haplorhini
    Immune Sera
    Insulin
    Iodine Radioisotopes
    Islets of Langerhans
    Maternal-Fetal Exchange
    Pancreas
    Pituitary Gland
    Pregnancy
    Tolbutamide

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    4974624

    Citation

    Mintz, D H., et al. "Fetal Insulin and Growth Hormone Metabolism in the Subhuman Primate." The Journal of Clinical Investigation, vol. 48, no. 1, 1969, pp. 176-86.
    Mintz DH, Chez RA, Horger EO. Fetal insulin and growth hormone metabolism in the subhuman primate. J Clin Invest. 1969;48(1):176-86.
    Mintz, D. H., Chez, R. A., & Horger, E. O. (1969). Fetal insulin and growth hormone metabolism in the subhuman primate. The Journal of Clinical Investigation, 48(1), pp. 176-86.
    Mintz DH, Chez RA, Horger EO. Fetal Insulin and Growth Hormone Metabolism in the Subhuman Primate. J Clin Invest. 1969;48(1):176-86. PubMed PMID: 4974624.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Fetal insulin and growth hormone metabolism in the subhuman primate. AU - Mintz,D H, AU - Chez,R A, AU - Horger,E O,3rd PY - 1969/1/1/pubmed PY - 1969/1/1/medline PY - 1969/1/1/entrez SP - 176 EP - 86 JF - The Journal of clinical investigation JO - J. Clin. Invest. VL - 48 IS - 1 N2 - The concentrations of plasma glucose, insulin, growth hormone, and immunoreactive growth hormone-like substance in subhuman primate fetal and maternal plasma were examined after the intravascular administration of glucose, arginine, or tolbutamide to the fetus. Cannulation of interplacental vessels permitted studies on the fetus in utero without disruption of fetal-placental-maternal anatomic integrity. Single glucose injections, glucose infusions, and arginine infusions into the fetus did not alter fetal plasma insulin concentrations. In contrast, tolbutamide injections elicited an immediate 3-4-fold increase in fetal plasma insulin concentrations. A bidirectional placental transfer of insulin was demonstrated with the use of simultaneously injected insulin-(125)I to the mother and insulin-(131)I to the fetus. Simian fetal plasma contained a substance which cross-reacted with immunologic identity to human growth hormone. In contrast, simian maternal plasma and amniotic fluid reacted with immunologic nonidentity to human growth hormone. Although glucose administration to the fetus did not suppress nor did arginine infusion consistently augment fetal plasma growth hormone levels, the latter were observed to vary in individual experiments. The plasma responses to the same stimuli in the neonate were also examined. In contrast to the fetal experiments, glucose injection in the neonate elicited a delayed rise in the concentration of plasma insulin. Similar to the fetus, the plasma concentration of insulin increased after tolbutamide injection and did not change in response to arginine infusion. The initial concentrations of neonatal plasma growth hormone were significantly lower when contrasted with the initial fetal plasma levels. There was no difference in the responsiveness of the fetal and neonatal growth hormone-releasing mechanisms when challenged by glucose or arginine infusion. The data indicate that the fetal plasma concentration of growth hormone is labile, that fetal growth hormone metabolism may differ from that in the neonate, and that pancreatic islet cell responsiveness rapidly changes after delivery. SN - 0021-9738 UR - https://www.unboundmedicine.com/medline/citation/4974624/Fetal_insulin_and_growth_hormone_metabolism_in_the_subhuman_primate_ L2 - https://doi.org/10.1172/JCI105966 DB - PRIME DP - Unbound Medicine ER -