THE EFFECT OF THE ADRENAL CORTEX ON CARBOHYDRATE METABOLISM1

Abstract

It appeared possible that an inability to form glucose from intermediate products of carbohydrate metabolism as well as from protein catabolism could account for many of the abnormalities observed in adrenal cortical insufficiency. Adrenalectomized, phlorhizin-treated rats were observed to have an impaired ability to form glucose from lactic acid, pyruvic acid or alanine; an increased utilization of available glucose; and a decreased ketonuria, glycosuria, N excretion, and D:N ratio. Adrenalectomized dogs showed a decreased glycemic response to epinephrin; an increased sensitivity to insulin; and a decreased threshold for signs of hypoglycemia. The adm. of 17-hydroxy-ll-dehydro-corticosterone or adrenal cortical extract restored the ability of adrenalectomized, phlorhizin-treated rats to form glucose from lactic acid, pyruvic acid and alanine; decreased the utilization of available glucose; and increased the ketonuria, glycosuria, nitrogen excretion, and glucose:nitrogen ratio. The adm. of corticosterone, 17-hydroxy-ll-dehydro-corticosterone or adrenal cortical extract resulted in a lowered R.Q., an increased N excretion, an increased blood glucose level and increased threshold for signs of hypoglycemia in adrenalectomized, insulin-treated dogs. Ability of adrenalectomized animals to convert three-carbon-atom intermediate substance of carbohydrate and protein metabolism to glucose or glycogen is markedly impaired. This defect may account for the rapid development of hypoglycemia in these animals following a prolonged fast, the adm. of insulin or phlor-hizin treatment.