Fetal metabolic response to endogenous insulin release.
The fetal metabolic response to tolbutamide-induced insulin release was evaluated in nine chronically catheterized fetal lambs. Tolbutamide produced an elevation in fetal insulin that persisted throughout the 1-hour experimental period (peak insulin concentration achieved was 76.1 +/- 9.5 micro U/ml). Fetal hyperinsulinemia was associated with a fall by 30 minutes in both fetal arterial and umbilical venous glucose concentrations as well as an increase in the umbilical glucose venous-arterial difference. This increase was associated with an elevation of fetal glucose uptake 65.6% +/- 29.6% above control at 30 minutes after infusion. Fetal arterial oxygen content fell after tolbutamide administration and was accompanied by an increase in the umbilical venous-arterial oxygen content difference (13.0% +/- 5.0% above the basal level.) Despite the increased venous-arterial difference, however, no change in umbilical oxygen consumption was noted. Isolated endogenous fetal insulin release is thus associated with a relatively rapid increase in umbilical glucose uptake as well as concomitant fetal hypoglycemia. The etiology of the mild fetal hypoxemia produced is unclear. The alterations in fetal glucose uptake in the ovine fetus after tolbutamide mimic those changes occurring after fetal exogenous insulin infusion. These alterations strongly suggest a significant role for insulin in the modulation of fetal carbohydrate metabolism and perhaps oxygen utilization.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D005260:Female; D005312:Fetal Blood / Q000032:analysis; D005333:Fetus / Q000378:metabolism*; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D000078790:Insulin Secretion; D010100:Oxygen / Q000097:blood; D011247:Pregnancy; D012756:Sheep; D014044:Tolbutamide / Q000494:pharmacology*; D014469:Umbilical Arteries; D014471:Umbilical Veins
D001786:Blood Glucose; D007328:Insulin; D014044:Tolbutamide; D010100:Oxygen