Epinephrine is not critical to prevention of hypoglycemia during exercise in humans

Epinephrine is not critical to prevention of hypoglycemia during exercise in humans BASED ON STUDIES in normal humans (17), we have concluded that the homeostatic adaptations that normally match increased glucose utilization and glucose production and prevent hypoglycemia moderate are the result of changes in the activities of redundant glucoregulatory systems, including activation of the sympathochromaffin system (28) and changes in pancreatic islet hormone secretion. Sympathochromaffin catecholamine release plays a primary role. Changes in islet hormones are not normally critical but decrements in insulin, increments in glucagon, or both become critical when catecholamine action is deficient. fails, and hypoglycemia can develop, when catecholamine action is blocked and changes in islet horEl04 0193-1849/86 $1.50 Copyright mones do not occur . The experimental design used in our previous studies (17) did not permit distinction between the roles of sympathetic neural and adrenomedullary catecholamines. Because of the rapidity of the catecholamine effects on glucose kinetics, because plasma epinephrine (1, 9) and norepinephrine (31) elevations of the magnitude observed early (17) would not be expected to exert substantial effects on glucose metabolism, and, because epinephrine-deficient (bilaterally adrenalectomized, glucocorticoid and mineralocorticoid replaced) humans have been reported to maintain euglycemia (US), we reasoned that norepinephrine released from sympathetic postganglionic neurons within the tissues is the relevant http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Endocrinology and Metabolism The American Physiological Society

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Publisher
The American Physiological Society
Copyright
Copyright © 1986 the American Physiological Society
ISSN
0193-1849
eISSN
1522-1555
Publisher site
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Abstract

BASED ON STUDIES in normal humans (17), we have concluded that the homeostatic adaptations that normally match increased glucose utilization and glucose production and prevent hypoglycemia moderate are the result of changes in the activities of redundant glucoregulatory systems, including activation of the sympathochromaffin system (28) and changes in pancreatic islet hormone secretion. Sympathochromaffin catecholamine release plays a primary role. Changes in islet hormones are not normally critical but decrements in insulin, increments in glucagon, or both become critical when catecholamine action is deficient. fails, and hypoglycemia can develop, when catecholamine action is blocked and changes in islet horEl04 0193-1849/86 $1.50 Copyright mones do not occur . The experimental design used in our previous studies (17) did not permit distinction between the roles of sympathetic neural and adrenomedullary catecholamines. Because of the rapidity of the catecholamine effects on glucose kinetics, because plasma epinephrine (1, 9) and norepinephrine (31) elevations of the magnitude observed early (17) would not be expected to exert substantial effects on glucose metabolism, and, because epinephrine-deficient (bilaterally adrenalectomized, glucocorticoid and mineralocorticoid replaced) humans have been reported to maintain euglycemia (US), we reasoned that norepinephrine released from sympathetic postganglionic neurons within the tissues is the relevant

Journal

AJP - Endocrinology and MetabolismThe American Physiological Society

Published: Jul 1, 1986

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