Inhibition of Phosphorylase With Cortisone and Its Activation With Adrenaline in the Rabbit

Since Browne, in 1943, demonstrated that adrenocorticotropic hormone or ACTH reduces glucose tolerance and causes glycosuria in connection with glucose tolerance test in man, a comprehensive literature on the subject has appeared. Long (1947) was the first to state that ACTH effect arises through stimulation of the adrenal cortex which releases steroids active in carbohydrate metabolism. Of these steroids, or glyco-corticoids, ll-dehydro-17-hydroxycorticosterone or compound E, also called cortisone, has become widely used as a therapeutic preparation. Ingle and associates (1945–46) first showed that prolonged glycosuria and hyperglycemia can be produced with cortisone. Alimentary, insulin-resistant diabetes, unaccompanied by acidosis, may also develop. There are a great number of reports dealing with this question too. In adrenalectomized animals the glycogen content of the liver can be restored with cortisone, and even over compensated (Olson et al. 1944, Venning et al. 1946). Teilum and associates (1950) produced intense glycogen deposition in the liver and kidneys of rabbits with large doses of cortisone.