A considerable amount of species variation exists in the relative hyperglycemic activities of catecholamines. For example, epinephrine (EPI) is a potent hyperglycemic agent in all mammalian species, whereas isoproterenol (ISO) has strong hyperglycemic activity in dogs, moderate activity in baboons, weak activity in rabbits, and relative inactivity in normal fed rats.1.2 Moreover, in rabbits there are differences between the in vitro glucose mobilizing activities of catecholamines as compared to in vivo effects.3 This suggests that there may be important indirect determinants of hyperglycemic activity that account for the species variation in the relative hyperglycemic activities of catecholamines. Previous work from our laboratory has shown that the hyperglycemic effect of ISO in rats is limited by its stimulating effect on insulin release.4 On the basis of indirect evidence, Sokal and Sarcione5 suggested that the hyperglycemia produced by EPI is mediated through increased glucagon release. Since catecholamines have been shown to release the potent glycogenolytic and gluconeogenic hormone, glucagon,6 it seems appropriate to examine the involvement of glucagon as well as insulin in the production of hyperglycemia by catecholamines in a variety of laboratory animals. We have hypothesized that pancreatic hormone release is an important determinant of catecholamine-induced hyperglycemia, and different patterns of pancreatic hormone release may explain, in part, the differences in the relative hyperglycemic activities of catecholamines that occur within and between species.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism