Regulation of pancreatic polypeptide secretion in the isolated perfused human pancreas
Abstract
The isolated perfused human pancreas was used as a model to assess factors mediating the pancreatic polypeptide cell response to glucose, insulin, gastric inhibitory polypeptide, and splanchnic nerve stimulation. Pancreases obtained from 18 cadaveric organ donors were isolated and perfused by way of the splenic artery utilizing a Krebs bicarbonate buffer in a single-pass perfusion system. Hormonal stimulation and inhibition of pancreatic polypeptide secretion were assessed, as was the influence of direct electrical stimulation of celiac neural fibers innervating the pancreas. In this in vitro human model, pancreatic polypeptide cell secretion was inhibited by hyperglycemia, although the presence of gastric inhibitory polypeptide augmented the pancreatic polypeptide cell response. Perfusion with low levels of insulin and splanchnic nerve stimulation augmented the response of the pancreatic polypeptide cell to hyperglycemia and gastric inhibitory polypeptide. Since the immunoreactive pancreatic polypeptide response was augmented when insulin and somatostatin release was inhibited by perfusion insulin or nerve stimulation, we conclude that the pancreatic polypeptide cell is regulated by the ambient degree of somatostatin release, insulin release, or both. These findings support a centrifugal pattern of intraislet blood flow.
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This is the first report clearly describing in vivo suppression of pancreatic polypeptide by physiological hyperinsulinaemia.
“Although previous studies have suggested the possibility that pancreatic polypeptide is suppressed by endogenous insulin secretion in vivo [36], or modulated by hyperinsulinaemia in vitro [37], to the best of our knowledge, this is the first report clearly describing such an effect in vivo.”
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Fanelli, C., Pampanelli, S., Epifano, L., Rambotti, A. M., Ciofetta, M., Modarelli, F., Di Vincenzo, A., Annibale, B., Lepore, M., Lalli, C., et al. (1994) · Diabetologia · doi:10.1007/bf00404337 · Cited by 193 · see citing works
Ca<sup>2+</sup>Signaling in Mouse Pancreatic Polypeptide Cells<sup>1</sup>
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- Authors
- Brunicardi, F. C., Druck, P., Sun, Y. S., Elahi, D., Gingerich, R. L., & Andersen, D. K.
- Affiliations
- State University of New York (US)
- Corresponding author
- Andersen, Dana K.
- ORCID
- Andersen, Dana K.
- Venue
- The American Journal of Surgery
- Publisher
- Elsevier BV
- Published
- 1988-01
- Volume
- 155
- Issue
- 1
- Pages
- 63-69
- ISSN
- 0002-9610 (ISSN-L)
- OpenAlex
- W2037620637
- Cited by
- 31
- References
- 28
- Citations by year
- 2024: 1 · 2023: 1 · 2021: 1 · 2019: 2 · 2018: 1 · 2016: 1 · 2015: 1 · 2014: 2
- FWCI
- 1.71
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The American Journal of Surgery (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01am030336-03)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Health Sciences › Medicine › Epidemiology › Neuroendocrine Tumor Research Advances
- Keywords
- pancreatic polypeptide, hyperglycemia, insulin, glucose-dependent insulinotropic polypeptide, splanchnic nerve stimulation, somatostatin, celiac plexus, pancreatic islets
- MeSH terms
- Adolescent, Adult, Age Factors, Female, Gastric Inhibitory Polypeptide, Glucose, Humans, Insulin, Male, Middle Aged, Pancreas, Pancreatic Polypeptide, Perfusion, Splanchnic Nerves, In Vitro Techniques
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