Insulin hypoglycemia, cerebral metabolism, and neural function in fetal lambs

The effect of insulin-induced hypoglycemia on cerebral oxidative metabolism (CMR(O₂)) was studied in nine late gestational fetal lambs using the radiolabeled microsphere technique for cerebral blood flow and brachiocephalic to sagittal sinus blood O₂ content differences. After 4 h insulin infusion to the fetus, arterial glucose fell from control levels of 0.96 ± 0.11 (SE) to 0.69 ± 0.09 mmol.l^-1.CMR(O₂) was reduced from 199 ± 23 to 155 ± 22 μmol.100 g^-1.min^-1 (P<0.05) and cerebral glucose uptake fell from 31 ± 4 to 25 ± 4 μmol.100 g^-1.min^-1 (P<0.02). During both euglycemia and hypoglycemia, 6 μmol glucose were taken up for each micromole of O₂, indicating that glucose was the sole metabolic substrate for oxidative metabolism. Although there was no change in fetal electrocortical activity during the hypoglycemia, fetal breathing movements were present only 19.4 ± 3.4% of the hypoglycemic hours compared with 36.8 ± 2.6% of the control period (P≤0.01). These results suggest that during rapidly induced fetal hypoglycemia, blood-brain barrier transport of glucose can limit cerebral glucose and O₂ uptake, and this decrease in cerebral metabolism is associated with a lowered incidence of fetal breathing movements.