The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Intra-islet insulin permits glucose to directly suppress pancreatic A cell function.
Open accessAbstract
Inhibition of pancreatic glucagon secretion during hyperglycemia could be mediated by (a) glucose, (b) insulin, (c) somatostatin, or (d) glucose in conjunction with insulin. To determine the role of these factors in the mediation of glucagon suppression, we injected alloxan while clamping the arterial supply of the pancreatic splenic lobe of dogs, thus inducing insulin deficiency localized to the ventral lobe and avoiding hyperglycemia. Ventral lobe insulin, glucagon, and somatostatin outputs were then measured in response to a stepped IV glucose infusion. In control dogs glucagon suppression occurred at a glucose level of 150 mg/dl and somatostatin output increased at glucose greater than 250 mg/dl. In alloxan-treated dogs glucagon output was not suppressed nor did somatostatin output increase. We concluded that insulin was required in the mediation of glucagon suppression and somatostatin stimulation. Subsequently, we infused insulin at high rates directly into the artery that supplied the beta cell-deficient lobe in six alloxan-treated dogs. Insulin infusion alone did not cause suppression of glucagon or stimulation of somatostatin; however, insulin repletion during glucose infusions did restore the ability of hyperglycemia to suppress glucagon and stimulate somatostatin. We conclude that intra-islet insulin permits glucose to suppress glucagon secretion and stimulate somatostatin during hyperglycemia.
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“These opponents interact not only with each other through the intra-islet insulin axis378, 379, 380, 381 but also with other organs/tissues, that is, the brain, liver, gut as well as insulin-dependent adipose and muscle tissues.”
From Pancreatic regulation of glucose homeostasis. (2016) · cites this paper as [379]
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Citations
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Metadata
- Authors
- Greenbaum, C. J., Havel, P. J., Taborsky, G. J., & Klaff, L. J.
- Affiliations
- United States Department of Veterans Affairs (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1991-09-01
- Volume
- 88
- Issue
- 3
- Pages
- 767-773
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC295460
- OpenAlex
- W2158603877
- Cited by
- 106
- References
- 46
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 4 · 2023: 3 · 2021: 8 · 2020: 3 · 2018: 3 · 2017: 3 · 2016: 7 · 2015: 3 · 2014: 5 · 2013: 3 · 2012: 4
- FWCI
- 0.50
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- American Diabetes Association
- National Institutes of Health (2r01dk012829-36, 1f32dk008211-01a1)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 12829, DK-08211, DK-17047, P30DK017047)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › 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
- glucagon suppression, somatostatin, hyperglycemia, pancreatic A cells, glucose infusion, pancreatic islets, glucagon secretion
- MeSH terms
- Insulin Secretion, Alloxan, Animals, Arginine, Dogs, Glucagon, Glucose, Hyperglycemia, Insulin, Islets of Langerhans, Somatostatin
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