Cerebral lactate metabolism in near-term fetal sheep.
The present study was designed to see if lactate can cross the blood-brain barrier of the near-term fetal sheep and replace glucose as an oxidative substrate during normoglycemia and acute insulin-induced hypoglycemia. Cerebral uptake of glucose, oxygen, lactate, and [14C]lactate as well as cerebral production of 14CO2 were measured under three conditions: 1) normoglycemia-normolactemia, 2) acute hypoglycemia-normolactemia, and 3) hypoglycemia-steady-state hyperlactemia. Although uptake of tracer [14C]lactate was consistent, there was no net uptake of unlabeled lactate during either normoglycemia or hypoglycemia. When arterial lactate concentration was raised from 2.2 +/- 0.5 to 3.3 +/- 0.4 (SE) mM by sodium lactate infusion, however, lactate was taken up. Comparison of cerebral [14C]lactate uptake with 14CO2 production indicated that the principal metabolic fate of lactate is oxidation. At increased concentrations, exogenous lactate accounted for approximately 7% of cerebral oxygen consumption. This study demonstrates that lactate crosses the blood-brain barrier of the near-term fetal sheep, is oxidized, and at elevated concentrations can partially replace glucose as an oxidative substrate during acute hypoglycemia.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001921:Brain / Q000196:embryology*; D005260:Female; D005333:Fetus / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism; D007773:Lactates / Q000097:blood / Q000378:metabolism*; D019344:Lactic Acid; D010101:Oxygen Consumption; D011247:Pregnancy; D012756:Sheep
D001786:Blood Glucose; D007773:Lactates; D019344:Lactic Acid; D005947:Glucose