Cerebral metabolic rate of oxygen:
Consumption = Cerebral blood flow x arterio-venous oxygen content difference = 3-6 ml oxygen/100 g per minute
Oxygen consumption is higher in the cortex than in the white matter. Under physiological conditions, cerebral metabolic consumption of oxygen is relatively stable, irrespective of whether the subject is asleep or engaged in intense mental activity.
D-glucose is the sole energy substrate of the brain, except in states of ketosis, when ketone bodies derived from the catabolism of non-esterified fatty acids in the liver can be utilised. Ketone body uptake into the brain is mediated by the monocarboxylic acid transporter-1. The brain consumes about 100-120g of glucose per day, equivalent to 60% of total hepatic production. Glucose oxidation in the CNS accounts for 20% of whole-body oxygen consumption.
D-glucose is transported into the brain by facilitated diffusion across the blood-brain barrier, involving membrane-based carrier mechanisms specific for D-glucose. Glucose uptake is mediated by glucose transporter-1, expressed at high density in the capillary endothelium, in an insulin-independent action. The glucose transporter-3 is responsible for glucose uptake into the neurons, and is also insulin-independent. There is a tight coupling between cerebral metabolic demand and cerebral substrate supply, which is in turn regulated by cerebral blood flow. Functional imaging demonstrates regionally specific increases in metabolism with cognitive, motor or visual activation. As glycogen stores in the brain are negligible, acute lowering of glucose causes the rapid onset of severe compromise of brain function.
The metabolic rate is reduced in sleep, coma, general anaesthesia and hypothermia.
The metabolic rate is increased with sensory stimulation, epileptiform activity, mental concentration, ketamine anaesthesia and hyperthermia.
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