The influence of insulin upon the metabolism of glucose by the brain

Abstract

Rapidly induced, sustained hyperglycaemia in rats caused a sharp, transient increase in cerebral glucose gain (defined as the rate at which glucose enters the brain from the circulating blood and is retained for metabolic or other purposes). This initial increase in gain during hyperglycaemia took place whether or not exogenous insulin was injected. However, if animals were not given insulin the increase in cerebral glucose gain was not sustained as the period of hyperglycaemia was prolonged, but decreased steadily until, after 20 min, it was similar to that found in animals with normal concentrations of glucose in the blood. The effect of the injection of insulin was to cause the initial sharp increase in the cerebral gain of glucose to be sustained (though at a somewhat lower level) during periods of hyperglycaemia lasting up to at least 60 min. Insulin did not act by blocking the efflux of glucose from the brain nor did it stimulate cerebral glucose metabolism indirectly by reducing the supply of ketone bodies to the brain. The concentration of glycogen in the brains of hyperglycaemic animals was almost doubled by insulin, but this increase in glycogen content only accounted for a small part of the extra glucose gained by the brains. Anaerobic glycolysis in the brain was not altered by insulin. It was concluded that insulin caused the cerebral cells to use more glucose not only to form glycogen but, to a much greater extent, to synthesize other substances, probably mainly the non-essential amino acids.