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
AJP - Endocrinology and Metabolism – The American Physiological Society
Published: Jul 1, 1986
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