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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Cites
Morgan, C. R., & Lazarow, A. (1963) · Diabetes · doi:10.2337/diab.12.2.115 · Cited by 2,197
DRUGS PRODUCING DIABETES THROUGH DAMAGE OF THE INSULIN SECRETING CELLS
Rerup, C. (1970) · Pharmacological Reviews · doi:10.1016/s0031-6997(25)06885-1 · Cited by 731
New Perspectives on the Microvasculature of the Islets of Langerhans in the Rat
Bonner‐Weir, S., & Orci, L. (1982) · Diabetes · doi:10.2337/diab.31.10.883 · Cited by 482
Unger, R. H., & Grundy, S. M. (1985) · Diabetologia · doi:10.1007/bf00273856 · Cited by 452
Glucagon physiology and pathophysiology in the light of new advances
Unger, R. H. (1985) · Diabetologia · doi:10.1007/bf00281991 · Cited by 361
Interplay of Nutrients and Hormones in the Regulation of Insulin Release*
PIPELEERS, D. G., Schuit, F. C., Veld, P. I. '., Maes, E., Hooghe-Peters, E. L., Winkel, M. V. D., & Gepts, W. (1985) · Endocrinology · doi:10.1210/endo-117-3-824 · Cited by 357
Effect of chronic hyperglycemia on in vivo insulin secretion in partially pancreatectomized rats.
Rossetti, L., Shulman, G. I., Zawalich, W. S., & DeFronzo, R. A. (1987) · Journal of Clinical Investigation · doi:10.1172/jci113157 · Cited by 330
Kaestner, K. H., Christy, R. J., McLenithan, J. C., Braiterman, L. T., Cornelius, P. K., Pekala, P. H., & Lane, M. D. (1989) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.86.9.3150 · Cited by 305
Insulin within islets is a physiologic glucagon release inhibitor
Maruyama, H., Hisatomi, A., Orci, L., Grodsky, G. M., & Unger, R. H. (1984) · Journal of Clinical Investigation · doi:10.1172/jci111658 · Cited by 303
Alloxan: history and mechanism of action
Lenzen, S., & Panten, U. (1988) · Diabetologia · doi:10.1007/bf02341500 · Cited by 250
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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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