Glucose transfer into rat brain during acute and chronic hyperglycemia

Abstract

Chronic hyperglycemia has been reported to decrease the maximum velocity of glucose transport across the blood-brain barrier by 30 to 40%. However, available measurements of brain glucose content during chronic hyperglycemia are consistent with an unaltered transport system. Because of this discrepancy the brain capillary permeability-surface area product (PA) was measured in awake-restrained rats during acute and chronic hyperglycemia. Acute hyperglycemia was produced by intraperitoneal injection of glucose, and chronic hyperglycemia was produced by treatment with streptozotocin. PA was measured using an intravenous tracer method. PA decreased during hyperglycemia, consistent with saturation kinetics for transfer. However, PA was similar in acutely and chronically hyperglycemic rats. These data suggest that down-regulation of facilitated glucose transport into the brain does not occur during chronic hyperglycemia.