Direct alpha-adrenergic stimulation of hepatic glucose production in human subjects
Abstract
Six normal humans each underwent infusions of 1) saline; 2) propranolol; 3) somatostatin; 4) somatostatin with propranolol; and 5) somatostatin with propranolol plus phentolamine on separate occasions. Propranolol alone had no effect on glucose production or plasma glucose. Somatostatin alone produced the expected initial decrease followed by an increase in both hepatic glucose production and plasma glucose. beta-Adrenergic blockade with propranolol displaced the glucose production (MANOVA, P = 0.0220) and plasma glucose (MANOVA, P = 0.0057) somatostatin response curves to higher levels, whereas alpha-adrenergic blockade with phentolamine combined with beta-adrenergic blockade displaced the glucose production (MANOVA, P = 0.0281) and plasma glucose (MANOVA, P = 0.0134) somatostatin response curves to lower levels. Because plasma insulin, C-peptide, and glucagon were suppressed comparably under all three conditions and plasma glucose concentrations were comparable initially, this represents direct alpha-adrenergic stimulation of hepatic glucose production in postabsorptive humans demonstrable when the primary glucoregulatory hormones are withdrawn and beta-adrenergic mechanisms are blocked. It is best attributed to sympathetic neural norepinephrine release.
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Maintenance of the postabsorptive plasma glucose concentration is a function of insulin and glucagon, not of insulin alone.
“These data provide further support for the concept that maintenance of the postabsorptive plasma glucose concentration is a function of insulin and glucagon, not of insulin alone”
From Epinephrine supports the postabsorptive plasma glucose concentration and prevents hypoglycemia when glucagon secretion is deficient in man (1984) · cites this paper as [13]
Combined α- and β-adrenergic blockade blunts the late increase in glucose production and plasma glucose that follows their initial decrease during combined insulin and glucagon deficiency produced by infusion of somatostatin.
“In an initial study (13) we found that combined α- and β-adrenergic blockade blunts the late increase in glucose production and plasma glucose that follows their initial decrease during combined insulin and glucagon deficiency produced by infusion of somatostatin.”
From Epinephrine supports the postabsorptive plasma glucose concentration and prevents hypoglycemia when glucagon secretion is deficient in man (1984) · cites this paper as [13]
Adrenergic blockade did not result in a progressive decline in plasma glucose in the initial study.
“Adrenergic blockade did not, however, result in a progressive decline in plasma glucose.”
From Epinephrine supports the postabsorptive plasma glucose concentration and prevents hypoglycemia when glucagon secretion is deficient in man (1984) · cites this paper as [13]
Cites
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Self-citationClutter, W. E., Bier, D. M., Shah, S. D., & Cryer, P. E. (1980) · Journal of Clinical Investigation · doi:10.1172/jci109840 · Cited by 576 · see citing works
Self-citationEpinephrine-induced insulin resistance in man
Deibert, D. C., & Defronzo, R. A. (1980) · Journal of Clinical Investigation · doi:10.1172/jci109718 · Cited by 560 · see citing works
Cyclic AMP and Aclrenergic Receptor Control of Rat Liver Glycogen Metabolism
SHERLINE, P., LYNCH, A., & GLINSMANN, W. H. (1972) · Endocrinology · doi:10.1210/endo-91-3-680 · Cited by 209 · see citing works
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Self-citationValverde, I., Dobbs, R., & Unger, R. H. (1975) · Metabolism · doi:10.1016/0026-0495(75)90095-5 · Cited by 92 · see citing works
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Intense Exercise Has Unique Effects on Both Insulin Release and Its Roles in Glucoregulation
Marliss, E. B., & Vranic, M. (2002) · Diabetes · doi:10.2337/diabetes.51.2007.s271 · Cited by 390 · see citing works
Glucoregulation during and after intense exercise: effects of beta-blockade.
Sigal, R. J., Purdon, C., Bilinski, D., Vranic, M., Halter, J. B., & Marliss, E. B. (1994) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.78.2.7906280 · Cited by 59 · see citing works
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Self-citationThe Prevention and Correction of Hypoglycemia
Cryer, P. E. (2001) · Comprehensive Physiology · doi:10.1002/cphy.cp070235 · Cited by 23 · see citing works
Self-citation
- Authors
- Rosen, S. G., Clutter, W. E., Shah, S. D., Miller, J. P., Bier, D. M., & Cryer, P. E.
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 1983-12-01
- Volume
- 245
- Issue
- 6
- Pages
- E616-E626
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2277112053
- Cited by
- 43
- References
- 6
- Citations by year
- 2025: 1 · 2023: 1 · 2021: 1 · 2020: 1 · 2017: 1 · 2016: 1 · 2013: 1
- FWCI
- 2.67
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- hepatic glucose production, alpha-adrenergic stimulation, somatostatin, propranolol, phentolamine, beta-adrenergic blockade, plasma glucose, glucoregulatory hormones, insulin, C-peptide, glucagon, postabsorptive state, glucose regulation
- MeSH terms
- Adult, Analysis of Variance, Blood Glucose, Blood Pressure, Drug Interactions, Female, Gluconeogenesis, Heart Rate, Humans, Liver, Male, Phentolamine, Propranolol, Receptors, Adrenergic, alpha, Somatostatin
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