PROTECTION BY LACTATE OF CEREBRAL FUNCTION DURING HYPOGLYCEMIA

Severe hypoglycaemia with brain dysfunction limits intensified therapy in patients with insulin-dependent diabetes mellitus, despite evidenc e that such therapy reduces the risk of chronic complications of the d isease. We have investigated the effect of infusing lactate (a potenti al non-glucose fuel for brain metabolism) on protective, symptomatic n eurohumoral responses and on brain function during hypoglycaemia in se ven healthy men. Elevation of lactate (within a physiological range) s ubstantially diminished catecholamines, growth hormone, cortisol, and symptomatic responses to hypoglycaemia and lowered the glucose level a t which these responses began. Glucagon responses were unaffected. Lac tate was also associated with a significant lowering of the glucose le vel at which brain function deteriorated, suggesting that brain functi on was protected during the hypoglycaemia. The defect in counter-regul ation is similar to that seen in hypoglycaemia-prone diabetic patients . Initiation of the protective responses to hypoglycaemia (except gluc agon) can be delayed by supporting-metabolism with an alternative meta bolic fuel. Cerebral cortical dysfunction of severe hypoglycaemia is a lso delayed. Our demonstration that higher brain function can be prote cted during hypoglycaemia may have therapeutic potential.