Cited by 106Pancreatic function and diabetesDiabetes Treatment and ManagementDiabetes and associated disorders

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Intra-islet insulin permits glucose to directly suppress pancreatic A cell function.

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Greenbaum, C J, Havel, P J, Taborsky, G J, Klaff, L J·1991·Journal of Clinical Investigation

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Abstract

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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Authors: Greenbaum, C. J., Havel, P. J., Taborsky, G. J., & Klaff, L. J.
Affiliations: United States Department of Veterans Affairs (US)
ORCID: Greenbaum, C J
Havel, P J
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 1991-09-01
Volume: 88
Issue: 3
Pages: 767-773
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci115375
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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Intra-islet insulin permits glucose to directly suppress pancreatic A cell function.

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