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Factors affecting the response to insulin in the normal subhuman pregnant primate.

Abstract

The concentrations of plasma glucose, free fatty acids, insulin, growth hormone, and placental prolactin in subhuman primate fetal and maternal plasma were examined following intravascular administration of insulin and glucagon to the fetus and mother. The neonatal plasma responses to these same stimuli were also examined. Fetal plasma glucose concentrations were minimally altered by direct fetal insulin injections, whereas neonatal glucose levels declined with similar injections. In both instances, however, plasma free fatty acid levels declined following insulin. When the amount of insulin given the fetus was increased, fetal plasma glucose concentrations did decline. Combined intravascular insulin injections and infusions in the mother were associated with a disappearance of the initial maternal to fetal plasma glucose concentration gradient and a nearly parallel fall in both maternal and fetal plasma glucose levels. It was concluded that insulin was biologically active in the fetus. Obtunded fetal plasma glucose responses to direct fetal insulin administration may be a function of placental transfer of glucose from the maternal pool. Maternal plasma placental prolactin and fetal plasma growth hormone levels were unchanged in the presence of sustained maternal and fetal hypoglycemia. However, neonatal plasma growht hormone levels did increase in response to hypoglycemia. The observed bidirectional placental barrier to transfer of radioisotopically labeled growth hormone indicated that fetal plasma growth hormone was solely of fetal origin. These data suggested further that a change in the growth hormone-releasing mechanism may occur from fetal to neonatal life. Direct maternal intravascular glucagon administration led to augmentation in both maternal and fetal plasma insulin and glucose levels. Direct fetal glucagon injections enhanced both maternal and fetal plasma insulin levels. These simultaneous changes in both plasma pools were consistent with the demonstration of a bidirectional placental transfer of radioisotopically labeled glucagon. The role of endogenously produced glucagon in these studies remains to be clarified.

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  • Authors

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    Source

    The Journal of clinical investigation 49:8 1970 Aug pg 1517-27

    MeSH

    Animals
    Blood Glucose
    Fatty Acids, Nonesterified
    Female
    Fetus
    Gestational Age
    Glucagon
    Growth Hormone
    Haplorhini
    Injections, Intravenous
    Insulin
    Iodine Isotopes
    Maternal-Fetal Exchange
    Placental Hormones
    Placental Lactogen
    Pregnancy
    Pregnancy, Animal
    Prolactin

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    4988208

    Citation

    Chez, R A., et al. "Factors Affecting the Response to Insulin in the Normal Subhuman Pregnant Primate." The Journal of Clinical Investigation, vol. 49, no. 8, 1970, pp. 1517-27.
    Chez RA, Mintz DH, Horger EO, et al. Factors affecting the response to insulin in the normal subhuman pregnant primate. J Clin Invest. 1970;49(8):1517-27.
    Chez, R. A., Mintz, D. H., Horger, E. O., & Hutchinson, D. L. (1970). Factors affecting the response to insulin in the normal subhuman pregnant primate. The Journal of Clinical Investigation, 49(8), pp. 1517-27.
    Chez RA, et al. Factors Affecting the Response to Insulin in the Normal Subhuman Pregnant Primate. J Clin Invest. 1970;49(8):1517-27. PubMed PMID: 4988208.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Factors affecting the response to insulin in the normal subhuman pregnant primate. AU - Chez,R A, AU - Mintz,D H, AU - Horger,E O,3rd AU - Hutchinson,D L, PY - 1970/8/1/pubmed PY - 1970/8/1/medline PY - 1970/8/1/entrez SP - 1517 EP - 27 JF - The Journal of clinical investigation JO - J. Clin. Invest. VL - 49 IS - 8 N2 - The concentrations of plasma glucose, free fatty acids, insulin, growth hormone, and placental prolactin in subhuman primate fetal and maternal plasma were examined following intravascular administration of insulin and glucagon to the fetus and mother. The neonatal plasma responses to these same stimuli were also examined. Fetal plasma glucose concentrations were minimally altered by direct fetal insulin injections, whereas neonatal glucose levels declined with similar injections. In both instances, however, plasma free fatty acid levels declined following insulin. When the amount of insulin given the fetus was increased, fetal plasma glucose concentrations did decline. Combined intravascular insulin injections and infusions in the mother were associated with a disappearance of the initial maternal to fetal plasma glucose concentration gradient and a nearly parallel fall in both maternal and fetal plasma glucose levels. It was concluded that insulin was biologically active in the fetus. Obtunded fetal plasma glucose responses to direct fetal insulin administration may be a function of placental transfer of glucose from the maternal pool. Maternal plasma placental prolactin and fetal plasma growth hormone levels were unchanged in the presence of sustained maternal and fetal hypoglycemia. However, neonatal plasma growht hormone levels did increase in response to hypoglycemia. The observed bidirectional placental barrier to transfer of radioisotopically labeled growth hormone indicated that fetal plasma growth hormone was solely of fetal origin. These data suggested further that a change in the growth hormone-releasing mechanism may occur from fetal to neonatal life. Direct maternal intravascular glucagon administration led to augmentation in both maternal and fetal plasma insulin and glucose levels. Direct fetal glucagon injections enhanced both maternal and fetal plasma insulin levels. These simultaneous changes in both plasma pools were consistent with the demonstration of a bidirectional placental transfer of radioisotopically labeled glucagon. The role of endogenously produced glucagon in these studies remains to be clarified. SN - 0021-9738 UR - https://www.unboundmedicine.com/medline/citation/4988208/Factors_affecting_the_response_to_insulin_in_the_normal_subhuman_pregnant_primate_ L2 - https://doi.org/10.1172/JCI106369 DB - PRIME DP - Unbound Medicine ER -