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Cited by 61Pancreatic function and diabetesDiabetes Management and ResearchDiabetes, Cardiovascular Risks, and Lipoproteins

Epinephrine and the regulation of glucose metabolism: effect of diabetes and hormonal interactions

Sherwin, Robert S., Shamoon, Harry, Hendler, Rosa, Saccà, Luigi, Eigler, Neil, Walesky, Mary·1980·Metabolism
DOI 10.1016/0026-0495(80)90024-4
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Abstract

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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Crossref · 10.1016/0026-0495(80)90024-4

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15 of 15 references verified0 citation errors · 0 not checkable

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  • A rapid rise of epinephrine can induce a transient elevation of hepatic glucose output, suppress endogenous insulin secretion, and directly inhibit insulin-stimulated glucose utilization.

    “Their paper cited the study of Sherwin et al. (42), in which the experiment showed that a rapid riseof epinephrine can induce a transient elevation of hepatic glucose output, suppress endogenous insulin secretion, and directly inhibit insulin-stimulated glucose utilization.”

    From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [42]

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Authors
Sherwin, R. S., Shamoon, H., Hendler, R., Saccà, L., Eigler, N., & Walesky, M.
Affiliations
Yale University (US)
Corresponding author
Sherwin, Robert S.
ORCID
Shamoon, Harry
Venue
Metabolism
Publisher
Elsevier BV
Published
1980-11
Volume
29
Issue
11
Pages
1146-1154
ISSN
0026-0495 (ISSN-L)
DOI
10.1016/0026-0495(80)90024-4
OpenAlex
W2034936478
Cited by
61
References
15
Citations by year
2026: 1 · 2025: 2 · 2024: 1 · 2023: 5 · 2022: 3 · 2021: 1 · 2020: 3 · 2019: 3 · 2018: 1 · 2016: 3 · 2015: 1 · 2014: 2 · 2013: 3
FWCI
2.84
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
epinephrine, glucose metabolism, diabetes mellitus, hyperglycemia, hepatic glucose production, insulin secretion, glucagon, cortisol, stress hyperglycemia, hormone crosstalk
MeSH terms
Adult, Animals, Blood Glucose, Diabetes Mellitus, Type 1, Dogs, Epinephrine, Fatty Acids, Nonesterified, Glucagon, Humans, Hydrocortisone, Insulin, Ketone Bodies, Liver, Metabolic Clearance Rate

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