TY - JOUR
T1 - Epinephrine and the regulation of glucose metabolism
T2 - Effect of diabetes and hormonal interactions
AU - Sherwin, Robert S.
AU - Shamoon, Harry
AU - Hendler, Rosa
AU - Saccà, Luigi
AU - Eigler, Neil
AU - Walesky, Mary
N1 - Funding Information:
From the Department of Internai Medicine, Yale University School of Medicine, New Haven, Corm. Supported in part by grants AM 20495 and RR 125 from the National Institutes of Health. Dr. Sherwin is the recipient of a Research Career Development Award (AM 00334) from the Naiional Institutes of Health. Address reprint requests to Robert S. Sherwin, M.D., Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, Conn. 06510. o 1980 by Grune Stratton, Inc. 0026&0495/80/2913-0008$01.00/0
PY - 1980
Y1 - 1980
N2 - Elevations of plasma epinephrine comparable to those observed in physiologic stress, cause a sustained 20–35 mg/dl elevation of plasma glucose in normal humans. This hyperglycemic action is due to a transient increase in hepatic glucose output as well as a reduction in the rate of glucose disposal which accounts for the persistence of hyperglycemia. The latter results from epinephrine-induced suppression of endogenous insulin secretion and, more importantly from a direct inhibitory effect on insulin-stimulated glucose utilization. In diabetes, the hyperglycemic effect of epinephrine is markedly accentuated. The enhanced rise in plasma glucose is due to an alternation in response of the liver to epinephrine. Despite infusion of insulin, epinephrine produces a sustained rather than transient elevation in hepatic glucose output in diabetic subjects. In contrast, the inhibitory effect of epinephrine on glucose utilization is unchanged by the diabetic state. In normal subjects, the hyperglycemic action of epinephrine is enhanced by simultaneous elevations of glucagon and cortisol. The former increases the magnitude, but not the duration, of the rise in hepatic glucose output induced by epinephrine. The latter, converts epinephrine's hepatic action from a transient to a sustained response. Our data thus suggest that marked hyperglycemia in normal subjects requires the concomitant elevation of multiple anti-insulin hormones, whereas such changes may occur in diabetes if any member of this group of hormones is increased. These findings may account for long-standing clinical observation that stress adversely affects blood glucose regulation to a much greater extent in diabetics as compared to normal subjects.
AB - Elevations of plasma epinephrine comparable to those observed in physiologic stress, cause a sustained 20–35 mg/dl elevation of plasma glucose in normal humans. This hyperglycemic action is due to a transient increase in hepatic glucose output as well as a reduction in the rate of glucose disposal which accounts for the persistence of hyperglycemia. The latter results from epinephrine-induced suppression of endogenous insulin secretion and, more importantly from a direct inhibitory effect on insulin-stimulated glucose utilization. In diabetes, the hyperglycemic effect of epinephrine is markedly accentuated. The enhanced rise in plasma glucose is due to an alternation in response of the liver to epinephrine. Despite infusion of insulin, epinephrine produces a sustained rather than transient elevation in hepatic glucose output in diabetic subjects. In contrast, the inhibitory effect of epinephrine on glucose utilization is unchanged by the diabetic state. In normal subjects, the hyperglycemic action of epinephrine is enhanced by simultaneous elevations of glucagon and cortisol. The former increases the magnitude, but not the duration, of the rise in hepatic glucose output induced by epinephrine. The latter, converts epinephrine's hepatic action from a transient to a sustained response. Our data thus suggest that marked hyperglycemia in normal subjects requires the concomitant elevation of multiple anti-insulin hormones, whereas such changes may occur in diabetes if any member of this group of hormones is increased. These findings may account for long-standing clinical observation that stress adversely affects blood glucose regulation to a much greater extent in diabetics as compared to normal subjects.
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U2 - 10.1016/0026-0495(80)90024-4
DO - 10.1016/0026-0495(80)90024-4
M3 - Article
C2 - 7001181
AN - SCOPUS:0019296119
SN - 0026-0495
VL - 29
SP - 1146
EP - 1154
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 11
ER -