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

B. S. Richardson, A. R. Hohimer, J. M. Bissonnette, C. M. Machida

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)R72-R77
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Issue number1
StatePublished - 1985

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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