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Failure of hydrocortisone to alter the transport of hexoses into rat brain and other tissues

THURSTON and PIERCE (1969) have studied the effects in vivo of the administration of hydrocortisone on the major energy-yielding components of cerebral metabolism, including phosphocreatine, ATP, glucose and glycogen. Young mice treated with hydrocortisone, 50 mg/kg subcutaneously for 10 days, exhibited a 2-fold increase in brain levels of glucose. Brain levels of phosphocreatine, glucose-6phosphate, and ATP were increased slightly, but brain levels of glycogen and lactate were unchanged. In discussing the mechanism of the dramatic increase in brain glucose, the authors considered several possibilities. Although the brain level of glucose increased to the degree seen with anaesthesia or with a block in both the hexose monophosphate shunt and the Krebs oxidative cycle, the absence of side effects to steroid administration led the authors to consider these possibilities unlikely. They suggested that the data could most likely be explained by an increase in the facilitated transport of glucose from the blood into the brain under the influence of hydrocortisone. Our present study was undertaken to explore this latter possibility as an extension of our interest in various factors affecting facilitated diffusion of hexoses in brain. In these experiments, we used two sugars, 3-O-methy~-~-glucose (3-MG) and 2-deoxy-D-glucose (2-DG), both of which enter brain by a carrier-dependent mechanism but neither of which support glycolysis (BUSCHIAZZO, TERRELL and REGEN, 1970). 3-MG is not metabolized, whereas 2-DG is phosphorylated only to 2-DG-I-phosphate. We studied both young and mature rats with steroid dosages similar to those used by THURSTON and PIERCE (1969). The transport of the hexoses into brain was analysed in terms of their brainlplasma ratios determined at various time intervals after intraperitoneal or intravenous injection.