Adrenergic influence on glucocounterregulation in man
Open accessAbstract
To investigate the adrenergic role in glucocounterregulatory mechanisms, single-blind randomised studies were performed in 7 normal males during severe insulin-induced hypoglycaemia with or without adrenergic blockade. Intravenous phentolamine administration (5 mg stat and 0.5 mg/min) did not interfere with the restoration of euglycaemia from hypoglycaemia. However, recovery of blood glucose in the presence of propranolol (3 mg/3 min and 0.8 mg/min) was retarded when compared with control studies (mean plasma glucose levels +/- SEM , 50 +/- 6 mg/dl versus 66 +/- 4 mg/dl at 120 min after insulin administration) despite appropriate glucagon, epinephrine, cortisol, and growth hormone responses. Plasma norepinephrine response was unaffected by propranolol but augmented threefold by phentolamine. Increases in plasma lactate, pyruvate and non-esterified fatty acids were blunted with propranolol while rebound non-esterified fatty acid was observed with phentolamine infusion. These data suggest that complete recovery of blood glucose from sever hypoglycaemia requires full sympathetic nervous system activity despite the integrity of other counterregulatory mechanisms.
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The adrenergic system regulates glucose recovery through activation of both alpha and beta receptors.
“The adrenergic system regulates glucose recovery through activation of both alpha and beta receptors, as supported by delayed glucose recovery during a single episode of hypoglycemia with administration of alpha and/or beta antagonists (29-31).”
From Plasma Epinephrine Contributes to the Development of Experimental Hypoglycemia-Associated Autonomic Failure (2020) · cites this paper as [31]
The Abstract reports that beta blockade with propranolol delayed glucose recovery after severe insulin-induced hypoglycaemia, supporting the beta-receptor part of the claim. It also reports that alpha blockade with phentolamine did not interfere with recovery, so this study does not support delayed recovery with alpha antagonism. The Discussion likewise emphasizes a role for beta-adrenergic mechanisms. (LLM, conf=0.90)
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- Authors
- Lilavivat, U., Brodows, R. G., & Campbell, R. G.
- Affiliations
- University of Rochester Medicine (US)
- ORCID
- Campbell, R.G.
- Venue
- Diabetologia
- Published
- 1981-04
- Volume
- 20
- Issue
- 4
- Pages
- 482-8
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W1997690681
- Cited by
- 27
- References
- 42
- Citations by year
- 2023: 1 · 2020: 1 · 2017: 1
- FWCI
- 6.18
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- National Institutes of Health (AM-20494)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- insulin-induced hypoglycemia, adrenergic blockade, propranolol, phentolamine, sympathetic nervous system, norepinephrine, free fatty acids, lactate, pyruvate, epinephrine, glucagon, cortisol, growth hormone
- MeSH terms
- Adult, Blood Glucose, Epinephrine, Fatty Acids, Nonesterified, Glucagon, Humans, Hydrocortisone, Insulin, Kinetics, Lactates, Male, Norepinephrine, Phentolamine, Propranolol, Pyruvates, Growth Hormone
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