The effect of hyperglycaemia on regional cerebral glucose oxidation in humans studied with [1-11C]-D-glucose.

Abstract

The effect of hyperglycaemia on regional cerebral glucose utilization was studied in five healthy males fasted over-night using positron emission tomography. Selectively labelled glucose, [1-11C]-D-glucose, was used as a tracer. After correction for the small loss of [11C]CO2 from the tissue, this tracer measures the rate of glucose oxidation rather than the total rate of glucose metabolism. Each subject was investigated twice: during normoglycaemia (plasma glucose 5.3 +/- 0.3 mumol mL-1) and at the end of a 2-h period of hyperglycaemia (plasma glucose 13.8 +/- 0.7 mumol mL-1). Assuming unchanged rate constant for loss of labelled CO2 at normo- and hyperglycaemia the oxidative metabolic rate of glucose was found to be slightly larger at combined hyperglycaemia and hypersulinemia (0.30 +/- 0.01 mmol mL-1 min-1) than at normal glucose and insulin levels (0.25 +/- 0.01 mmol mL-1 min-1). This suggests that the process of glucose phosphorylation might not be fully saturated in the human brain or, alternatively, that the glycogen deposition increases during short-term hyperglycaemia. The relative increase of oxidative metabolic rate was considerably larger (approximately 50%) in white matter than in the brain as a whole (20%). The brain glucose content was found to increase non-linearly with increasing plasma glucose. Together with data from previous studies these results suggest that the free glucose in the human brain is close to zero when the plasma glucose is below 2 mumol mL-1.