Human Fetal Insulin Response to Sustained Maternal Hyperglycemia

Obenshain, S. Scott; Adam, Peter A. J.; King, Katherine Callen; Teramo, K; Raivio, Kari O.; Räihä, Niels C. R.; Schwartz, Robert

doi:10.1056/nejm197009102831104

Cited by 113 publications

(23 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…An alteration in the normal circulating levels of one or both of these hormones in the immediate postnatal period may greatly hamper the metabolic adaptation [13]. Maternal glucose infusion by raising maternal blood glucose level facilitates diffusion of higher amounts of glucose across the placenta to the fetus and causes fetal hyperglycemia [2,5,17, 24] which in turn stimulates fetal insulin [2,9] and inhibits glucagon secretion [10]. Thus a significant increase in fetal/cord plasma insulin [4,11,15] and decrease in glucagon levels [3,11] occurs.…”

Section: Discussionmentioning

confidence: 99%

“…Experimental studies had shown that infusions of glucose to women prior to delivery causes maternal and transplacental hyperglycemia [2,5,12,17,24] and an increase in fetal insulin levels [2,5,15,17,24]. Prospective studies of infants whose mothers received glucose infusion during induction of epidural or general anesthesia prior to normal or cesarean section delivery, have also shown a rapid postnatal fall in blood glucose level of such infants [11,16].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effect of maternal intrapartum glucose therapy on neonatal blood glucose levels and neurobehavioral status of hypoglycemic term newborn infants

Singhi

1988

Jpme

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of maternal intrapartum glucose therapy on neonatal blood glucose levels and neurobehavioral status of hypoglycemic term newborn infants

Singhi

1988

Jpme

View full text Add to dashboard Cite

“…Several investigators have found that the L/S ratio is not a reliable predictor of lung maturation in pregnancies complicated by diabetes (1 5, 16). Because the fetus of the diabetic mother is known to be hyperinsulinemic, it has been proposed that the deleterious effects of maternal diabetes on the fetus are due to elevated fetal plasma insulin levels (17,18). In previous studies, we have shown that insulin, when added alone to serum-free medium, has no effect on surfactant phospholipid synthesis by human fetal lung tissue maintained in vitro (19,20).…”

Section: The Cecil H and Ida Green Center For Reproductive Biology Smentioning

confidence: 99%

The Concentration of the 35-kDa Surfactant Apoprotein in Amniotic Fluid from Normal and Diabetic Pregnancies

et al. 1988

View full text Add to dashboard Cite

ABSTRACT. A specific, enzyme-linked immunoabsorbent assay was used to determine the concentration of the 35,000 mol wt surfactant apoprotein (SP-A) in samples of amniotic fluid obtained from nondiabetic (n = 358) and diabetic (n = 29) women. The enzyme-linked immunoabsorbent assay was performed with rabbit antibodies directed against SP-A present in lavage fluid from a patient with alveolar proteinosis. Amniotic fluid SP-A concentrations increased as a function of gestational age, from <3 jtg/ml at 30-31 wk to 24 pg/ml at 40-41 wk, and were positively correlated with the lecithin to sphingomyelin ratio ( p < 0.01). SP-A concentrations also increased as a function of gestational age in shake test positive samples ( p < 0.05), but were unchanged in shake test-negative samples. There was no difference in the surfactant apoprotein concentration of male compared with female fetuses at any gestational age. In amniotic fluid obtained from 20 diabetic women, SP-A levels were significantly less than in nondiabetic pregnancies that were matched for gestational age and sex of the fetus ( p < 0.05). The SP-A concentrations in amniotic fluids obtained from nine women who were diabetic and hypertensive and from 10 hypertensive women were not different from matched controls. The relationships described above were valid whether the SP-A concentration was expressed per mg protein or per ml amniotic fluid. These data are suggestive that the concentration of amniotic fluid SP-A is decreased in diabetic pregnancies. (Pediafr Res 24: 728-734, 1988)

show abstract

“…In early gestation (13-18 weeks), the human fetal pancreas is relatively unresponsive to increases in maternal [25] and fetal [2] blood sugar although there is insulin present in fetal blood and preparations of the isolated human fetal pancreas release insulin when challenged with physiologic stimuli other than glucose [12,24]. The fetal pancreas of the rhesus monkey is also unresponsive to a glucose challenge [22].…”

Section: Introductionmentioning

confidence: 99%

Effect of Insulin and Epinephrine on the Carbohydrate Metabolism and Adenylate Cyclase Activity of Rhesus Fetal Muscle

1973

View full text Add to dashboard Cite

ExtractCarbohydrate metabolism of skeletal muscle from rhesus fetuses at 58% of gestation (95 days) is sensitive to epinephrine in vitro. Epinephrine increased lactate production and decreased glucose uptake, 14 C-lactate production, glycogen content, and 14 Cglycogen formation as well as 14 CC>2 production. These responses to epinephrine are similar to those in adult muscle. However, in some cases the magnitude of these responses appears lower in fetal muscle. The content of cyclic 14 C-adenosine 3',5'-monophosphate (cyclic 14 C-AMP) was about 2.5-fold higher in the 100-day fetal muscle than in the adult. Epinephrine stimulated adenylate cyclase activity almost threefold in fetal and fourfold in adult muscle. When incubated with muscle from 85-day fetal monkeys, insulin increased glucose uptake, lactate and lactate-14 C production, and 14 CO 2 production; the greatest effect was found in the increased incorporation of labeled glucose into glycogen. Both synthetase I and phosphorylase a activities were present at 78-80 days of fetal age. Our data show that as early as about 58% of term the carbohydrate metabolism of fetal rhesus muscle in vitro is sensitive to epinephrine and that the hormone probably acts through the adenylate cyclase and the "second messenger" system of cyclic AMP as it does in adult muscle. SpeculationOur data offer indirect evidence that insulin and epinephrine mediate glycogen metabolism via cyclic AMP in rhesus fetal muscle as early as 85 days of gestational age (52% of term) and that these hormones operate through similar enzyme systems in fetal and adult muscle. It is possible that glycogen synthetase and phosphorylase, or other enzymes mediating the cyclic AMP response, are not identical in fetal and adult muscle; fetal isoenzyme patterns for muscle lactate dehydrogenase differ markedly from those of the adult. However, it is difficult to reconcile the existence of major differences in the enzyme milieu in fetal and adult muscle with the similar overall actions of epinephrine and insulin on glycogenesis and glycogenolysis demonstrated in our experiments.

show abstract

Human Fetal Insulin Response to Sustained Maternal Hyperglycemia

Cited by 113 publications

References 19 publications

Effect of maternal intrapartum glucose therapy on neonatal blood glucose levels and neurobehavioral status of hypoglycemic term newborn infants

Effect of maternal intrapartum glucose therapy on neonatal blood glucose levels and neurobehavioral status of hypoglycemic term newborn infants

The Concentration of the 35-kDa Surfactant Apoprotein in Amniotic Fluid from Normal and Diabetic Pregnancies

Effect of Insulin and Epinephrine on the Carbohydrate Metabolism and Adenylate Cyclase Activity of Rhesus Fetal Muscle

Contact Info

Product

Resources

About