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Quantitative Determination of the Interaction Between Epinephrine and Various Insulin Releasers in Man
Abstract
Epinephrine significantly inhibited glucose-induced insulin release in man, the threshold dose being about 20 ng./kg. per minute. Maximal effect was attained with 60 ng./kg. per minute. In the presence of the threshold epinephrine dose, the dose-response curve for glucose-induced insulin release seemed to be displaced almost in parallel to the right of the control, suggesting competitive Inhibition. With the high epinephrine dose the inhibition of insulin release was of a noncompetitive nature. Epinephrine did not significantly suppress insulin release induced by either arginine or tolbutamide as compared with the effect of these insulinagogues when given at normoglycemia. Only in the case of glucagon did the high epinephrine dose (90 ng./kg. per minute) markedly inhibit the insulinogenic effect of the hormone (p<0.001) even when the effect of glucagon at normoglycemia was used as control. Since glucose exerted synergistk effects on insulin release in-duced by the other insulinagogues (arginine, glucagon, and tolbutamide), the insulinogenic effect of these insulinagogues In the presence of epinephrine was compared with their effect under hyperglycemie conditions similar to those obtained with epinephrine alone. It was found that epinephrine at a dose of 30 ng./kg. per minute totally inhibited the synergism between the hyperglycemie and the insulinagogues on insulin release. The greater the synergism—as with arginine and glucagon—the larger was the percentage inhibition by epinephrine. A threefold increase in the epinephrine dose further reduced the insulin response. Our experiments suggest that epinephrine—in the doses used—inhibited the effect of glucose on insulin release. This effect occurred regardless of whether glucose was used as the sole stimulator of insulin release or was used in synergism with such insulinagogues as arginine, tolbutamide, or glucagon.
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Human studies have confirmed that epinephrine represses endogenous insulin secretion.
“which remains debatable as human studies have confirmed the effect of epinephrine on repressing endogenous insulin secretion (39, 40).”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [40]
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Cited by
Sorted by citations
Halter, J. B., Graf, R. J., & Porte, D. (1979) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-48-6-946 · Cited by 150
Islet function and stress hyperglycemia: plasma glucose and epinephrine interaction
Halter, J. B., Beard, J. C., & Porte, D. (1984) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1984.247.1.e47 · Cited by 116
Davani, B., Portwood, N., Bryzgalova, G., Reimer, M. K., Heiden, T., Östenson, C., Okret, S., Åhrén, B., Efendić, S., & Khan, A. (2004) · Diabetes · doi:10.2337/diabetes.53.2007.s51 · Cited by 82
“Because catecholamine also inhibits arginineinduced insulin release (33), this finding is compatible with the hypothesis that increased signaling by 2-AR is involved in the regulation of insulin secretion in the -cells of TG mice.”
ResultSelf-citationInfluence of Small Increments of Epinephrine on Glucose Tolerance in Normal Humans
Hamburg, S., HENDLER, R., & SHERWIN, R. S. (1980) · Annals of Internal Medicine · doi:10.7326/0003-4819-93-4-566 · Cited by 57
Insulinotropic and gastrin-releasing action of gastrin-releasing peptide (GRP)
Greeley, G. H., & Thompson, J. C. (1984) · Regulatory Peptides · doi:10.1016/0167-0115(84)90164-2 · Cited by 51
Adrenaline inhibition of insulin release: role of the repolarization of the B cell membrane
Debuyser, A., Drews, G., & Henquin, J. C. (1991) · Pflügers Archiv - European Journal of Physiology · doi:10.1007/bf00372998 · Cited by 29
“Our in vitro findings may probably explain the observation that higher doses of adrenaline were required to inhibit tolbutamide- or arginine-induced insulin release than to inhibit glucose-induced release in man [12].”
BackgroundEffect of sympathetic blockade by spinal anesthesia on pancreatic islet function in man
Halter, J. B., & Pflug, A. E. (1980) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1980.239.2.e150 · Cited by 23
Das, V. A., Robinson, R., & Paulose, C. S. (2006) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-006-9142-6 · Cited by 15
“The increased sympathetic activity can inhibit the insulin secretion from the pancreatic islets [34, 35, 12].”
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Chronic hyperglycemia and insulin concentrations in fetal lambs
Lips, J. P., Jongsma, H. W., Crevels, J., & Eskes, T. K. A. B. (1988) · American Journal of Obstetrics and Gynecology · doi:10.1016/0002-9378(88)90530-3 · Cited by 11
On the pathogenesis of maturity-onset diabetes mellitus
Luft, R., & Efendić, S. (1978) · Acta Diabetologica · doi:10.1007/bf02581002 · Cited by 11
Self-citationThe effects of epinephrine on islet hormone secretion in the dog
Ahrén, B., Veith, R. C., & Taborsky, G. J. (1988) · International Journal of Pancreatology · doi:10.1007/bf02788471 · Cited by 9
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The progression of secondary diabetes: A review of modeling studies
Yang, B., Li, J., Haller, M. J., Schatz, D. A., & Rong, L. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.1070979 · Cited by 6
“The model was built upon the assumption that epinephrine can induce small net stimulation of insulin secretion from pancreatic b-cells, which remains debatable as human studies have confirmed the effect of epinephrine on repressing endogenous insulin secretion (39, 40).”
BackgroundEndogenous hyperglycemia restores insulin release impaired by somatostatin analogue
Taborsky, G. J., & Porte, D. (1981) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1981.240.4.e407 · Cited by 6
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Proportional inhibition of glucose-induced insulin release by somatostatin
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Type I Diabetes Mellitus (Insulin‐Dependent Diabetes Mellitus)
Rizza, R. A., Jensen, M. D., & Nair, K. S. (2001) · Comprehensive physiology · doi:10.1002/cphy.cp070236 · Cited by 1
“Thus insulin secretion increases as glucose concentrations rise, albeit not to the same extent as would occur in the absence of epinephrine (18, 70, 203, 221).”
Davani, B. (2003) · Figshare · Cited by 1
Endokrines System und Schock: Therapeutische Perspektiven
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Metadata
- Authors
- Efendić, S., Luft, R., & Cerasi, E.
- Affiliations
- Karolinska University Hospital (SE)
- ORCID
- Cerasi, Erol
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 1978-03-01
- Volume
- 27
- Issue
- 3
- Pages
- 319-326
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2120395965
- Cited by
- 23
- References
- 0
- Citations by year
- 2022: 1
- FWCI
- 4.65
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Vetenskapsrådet
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- epinephrine, insulin secretion, glucose-stimulated insulin secretion, L-arginine, tolbutamide, glucagon, competitive inhibition, non-competitive inhibition, hyperglycemia, dose-response relationship, insulin secretion inhibition
- MeSH terms
- Adult, Arginine, Dose-Response Relationship, Drug, Epinephrine, Female, Glucose, Humans, Insulin, Male, Middle Aged, Tolbutamide
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