Roles of glucagon and epinephrine in hypoglycemic and nonhypoglycemic glucose counterregulation in humans

P. E. Cryer, T. F. Tse, W. E. Clutter, S. D. Shah

Research output: Contribution to journalArticlepeer-review

34 Scopus citations

Abstract

Studies of two models of human glucose counterregulation, glucose recovery from insulin-induced hypoglycemia and the transition from exogenous glucose delivery to endogenous glucose production late after glucose ingestion, indicate that the principles of rapid hypoglycemic and nonhypoglycemic glucose counterregulation in these models are the same. 1) Neither is solely explicable on the basis of dissipation of insulin; 2) glucagon plays a primary counterregulatory role in both; 3) epinephrine compensates largely for deficient glucagon secretion in both; and 4) counterregulation fails to occur only in the absence of both glucagon and epinephrine in both. Thus, prevention as well as correction of hypoglycemia is effectively accomplished by redundant glucose counterregulatory systems, primarily glucagon and secondarily epinephrine, coupled with dissipation of insulin in humans. Other hormones, neural mechanisms, or autoregulation may be involved but need not be invoked and are not sufficiently potent to prevent or correct hypoglycemia when both of the key glucose counterregulatory hormones, glucagon and epinephrine, are deficient. Although confirmed in that they predict the impact of disease-related deficiencies of glucagon, epinephrine, or both, the extent to which these principles can be generalized to additional models of glucose counterregulation remains to be established. However, they provide a basis for plausible, testable hypotheses concerning the physiology and pathophysiology of glucose counterregulation.

Original languageEnglish
Pages (from-to)E198-E205
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume10
Issue number2
StatePublished - Jan 1 1984

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