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

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

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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  • Insulin and glucagon interact with each other through intra-islet insulin axis and with other organs/tissues (brain, liver, gut, adipose, muscle).

    “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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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)
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
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 › 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
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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