Insulin within islets is a physiologic glucagon release inhibitor
Open accessAbstract
To determine if glucagon secretion is under physiological control of intra-islet insulin, pancreata from normal rats were perfused at a 100 mg/dl glucose concentration with either guinea pig antiinsulin serum or normal guinea pig serum in a nonrecirculating system. Perfusion of antiserum was followed within 3 min by a significant rise in glucagon that reached peak levels three times the base-line values and assumed a hectic pattern that returned rapidly to base-line levels upon termination of the antiserum perfusion. Nonimmune guinea pig serum had no effect. To gain insight into the probable site of insulin neutralization, 125I-labeled human gamma-globulin was added to antiserum or nonimmune serum and perfused for 3 min. More than 83% of the radioactivity was recovered in the effluent within 3 min after termination of the infusion, and only 0.05 +/- 0.015% of the radioactivity injected was present in the pancreas 10 min after the perfusion. The maximal amount of insulin that could be completely bound to insulin antibody at a dilution and under conditions simulating those of the perfusion experiments was 20 mU/min. It is concluded that insulin maintains an ongoing restraint upon alpha cell secretion and in its absence causes hectic hypersecretion of glucagon. This restraint probably occurs largely in the intravascular compartment. Loss of this release-inhibiting action of insulin may account for initiation of hyperglucagonemia in insulin-deficient states.
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Surgery did not alter the inhibitory effects of glucose or insulin on α-cells.
“In our subjects, glucagon was suppressed by IV glucose in GB and control subjects alike, indicating that surgery did not alter the inhibitory effects of glucose or insulin on α-cells (26,27).”
From Gastric Bypass Surgery Enhances Glucagon-Like Peptide 1–Stimulated Postprandial Insulin Secretion in Humans (2011) · cites this paper as [27]
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- Authors
- Maruyama, H., Hisatomi, A., Orci, L., Grodsky, G. M., & Unger, R. H.
- Affiliations
- University of Geneva (CH)
- University of Texas Health Science Center at Dallas (US)
- ORCID
- Maruyama, H
- Venue
- Journal of Clinical Investigation
- Published
- 1984-12-01
- Volume
- 74
- Issue
- 6
- Pages
- 2296-2299
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC425424
- OpenAlex
- W1984541901
- Cited by
- 303
- References
- 17
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 5 · 2023: 5 · 2022: 1 · 2021: 15 · 2020: 10 · 2019: 9 · 2018: 11 · 2017: 12 · 2016: 14 · 2015: 10 · 2014: 15 · 2013: 6 · 2012: 8
- FWCI
- 9.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (2r01am022150-07)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- insulin, glucagon secretion, pancreatic islets, alpha cells, hyperglucagonemia, insulin deficiency, hypersecretion
- MeSH terms
- Animals, Glucagon, Guinea Pigs, Insulin, Insulin Antibodies, Islets of Langerhans, Male, Perfusion, Time Factors, Rats
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