This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by BENSON, J. W. Articles by ENSINCK, J. W. Search for Related Content PubMed PubMed Citation Articles by BENSON, J. W., JR. Articles by ENSINCK, J. W.

Glucagon and Catecholamine Secretion During Hypoglycemia in Normal and Diabetic Man

Department of Medicine, University of Washington, School of Medicine Seattle, Washington 98195

Reprint requests should be addressed to: John W. Ensinck, M.D., Department of Medicine, University of Washington, Seattle, Washington 98195.

To examine the role of catecholamines in glucopenia-induced glucagon secretion, urinary epinephrine and norepinephrine and plasma immunoreactive glucagon (IRG) were measuredduring insulin-induced hypoglycemia in normal and insulin-dependent diabetic man. Despite equivalent levels of hypoglycemia the mean plasma IRG increment in diabetics was only 15% of normals. The increases in epinephrine and norepinephrine were comparable in diabetics and normals; thus, the blunted response in plasma IRG to the stimulus of low blood sugar in diabetics cannot be explained by a generalized defect in catecholamine secretion. It is suggested that an alpha-cell glucoreceptor defect may account for the abnormal response to glucopenia in diabetics.

To evaluate the possibility that impaired sensitivity to circulating catecholamines could explain the alpha cell dysfunction in diabetics, exogenous epinephrine was infused in normals and insulindependent diabetics. Elevated plasma IRG during epinephrine infusion was observed in only 50% of normals. The diabetics were hyperresponsive; mean increment in plasma IRG 3 times that of normals. The data demonstrate enhanced rather than impaired sensitivity to catecholamines in diabetes mellitus.

Supported in part by the Clinical Research Center at the University of Washington (GCRC Grant RR-37) and by NIH grants AM-16008 and AM-17698. Dr. Benson is a recipient of a National Institutes of Health Research Fellowship (1-F22-AM02400-02). Dr. Johnson was supported by a ResearchCareer Development Award (1-K04-AM-70727).

Received July 9, 1976.

This article has been cited by other articles:

				D. C. SIMONSON, W. V. TAMBORLANE, R. A. DeFRONZO, and R. S. SHERWIN Intensive Insulin Therapy Reduces Counterregulatory Hormone Responses to Hypoglycemia in Patients with Type I Diabetes Ann Intern Med, August 1, 1985; 103(2): 184 - 190. [Abstract] [PDF]

				D. E. WILSON Excessive Insulin Therapy: Biochemical Effects and Clinical Repercussions: Current Concepts of Counterregulation in Type I Diabetes Ann Intern Med, February 1, 1983; 98(2): 219 - 227. [Abstract] [PDF]