Modification of Glucagon-Induced Hyperglycemia in Rats by 17-ethyl-19-nortestosterone

Abstract

Sensitivity of rats to glucagon (0.1 mg/kg body wt.) was tested in animals receiving 17-ethyl-19-nortesto-sterone (0.15 mg/rat/day) for 5 days. Additional glucagon-sensitivity tests were measured in rats receiving the steroid and cortisone concurrently, in steroid injected hypophysectomized rats, in castrated rats, and in testosterone-injected (0.15 mg/rat/day) rats. Analyses were made of blood glucose, phosphorus, urea, and both liver and testicular glycogen. The results indicate that the suppression of glucagon-induced hyperglycemia by the steroid 17-ethyl-19-nortesto-sterone is probably not mediated through the hypophysis, its target glands, or by blocking glycogenolytic pathways. Rather, evidence presented suggests that modification of glucagon action by the anabolic steroid is mediated by a suppression of gluconeogenesis.