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Brain oxygen utilization is unchanged by hypoglycemia in normal humans: lactate, alanine, and leucine uptake are not sufficient to offset energy deficit

¹Department of Internal Medicine, University of New Mexico, Albuquerque, New Mexico; and ²Department of Clinical and Experimental Medicine, University of Padova, Padua, Italy

Submitted 7 February 2005 ; accepted in final form 30 August 2005

During hypoglycemia, substrates other than glucose have been suggested to serve as alternate neural fuels. We evaluated brain uptake of endogenously produced lactate, alanine, and leucine at euglycemia and during insulin-induced hypoglycemia in 17 normal subjects. Cross-brain arteriovenous differences for plasma glucose, lactate, alanine, leucine, and oxygen content were quantitated. Cerebral blood flow (CBF) was measured by Fick methodology using N₂O as the dilution indicator gas. Substrate uptake was measured as the product of CBF and the arteriovenous concentration difference. As arterial glucose concentration fell, cerebral oxygen utilization and CBF remained unchanged. Brain glucose uptake (BGU) decreased from 36.3 ± 2.6 to 26.6 ± 2.1 µmol·100 g of brain^–1·min^–1 (P < 0.001), equivalent to a drop in ATP of 291 µmol·100 g^–1·min^–1. Arterial lactate rose (P < 0.001), whereas arterial alanine and leucine fell (P < 0.009 and P < 0.001, respectively). Brain lactate uptake (BLU) increased from a net release of –1.8 ± 0.6 to a net uptake of 2.5 ± 1.2 µmol·100 g^–1·min^–1 (P < 0.001), equivalent to an increase in ATP of 74 µmol·100 g^–1·min^–1. Brain leucine uptake decreased from 7.1 ± 1.2 to 2.5 ± 0.5 µmol·100 g^–1·min^–1 (P < 0.001), and brain alanine uptake trended downward (P < 0.08). We conclude that the ATP generated from the physiological increase in BLU during hypoglycemia accounts for no more than 25% of the brain glucose energy deficit.

brain uptake; brain glucose; amino acids; cerebral blood flow

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