Local cerebral glucose consumption during insulin-induced hypoglycemia, and in the recovery period following glucose administration.

Abstract

Using the 14C-deoxyglucose technique, we estimated local glucose consumption in the rat brain (1-CMRgl) in hypoglycemia of sufficient severity to cause cessation of spontaneous EEG activity, and in the recovery period following a 30 min period of such hypoglycemia. After 5 and 30 min of hypoglycemia. 1-CMRgl was markedly reduced in many cerebral structures (cerebral cortices, caudateputamen, thalamus, and hippocampus) but unchanged or only moderately reduced in other structures (cerebellar cortex, hypothalamus, and pontine grey). The results indicate that differences in 1-CMRgl were caused by regional differences in the true or apparent kinetic constants for glucose transport, or that the consequences of a hypoglycemic derangement of cellular metabolism interfered with glucose transport in some regions. Local CMRgl was markedly heterogenous in the recovery period, induced by glucose administration in animals with a prior (30 min) period of hypoglycemia. In general, a reduced posthypoglycemic glucose consumption was correlated to low 1-CMRgl values during hypoglycemia. However, the hippocampus provided an exception since its CMRgl returned to control values. A correlation with previous measurement of local cerebral blood flow (1-CBF) demonstrates that regions having a pronounced reduction in 1-CMRgl during hypoglycemia developed a mismatch between blood flow and metabolic rate in the recovery period, the flow showing a disproportional reduction.