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Cited by 79Pancreatic function and diabetesNeuropeptides and Animal PhysiologyDiabetes Treatment and Management

The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.

Inhibition of glucose stimulated insulin secretion by neuropeptide Y is mediated via the Y1 receptor and inhibition of adenylyl cyclase in RIN 5AH rat insulinoma cells

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Morgan, D. G., Kulkarni, R. N., Hurley, J. D., Wang, Z. L., Wang, R. M., Ghatei, M. A., Karlsen, A. E., Bloom, S. R., Smith, D. M.·1998·Diabetologia
DOI 10.1007/s001250051095
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Abstract

Neuropeptide Y (NPY) has been shown to inhibit insulin secretion from the islets of Langerhans. We show that insulin secretion in the insulinoma cell line RIN 5AH is inhibited by NPY. 125I-Peptide YY (PYY) saturation and competition-binding studies using NPY fragments and analogues on membranes prepared from this cell line show the presence of a single class of NPY receptor with a Y1 receptor subtype-like profile. Inhibition of insulin secretion in this cell line by NPY fragments and analogues also shows a Y1 receptor-like profile. Both receptor binding and inhibition of insulin secretion showed the same orders of potency with NPY > [Pro34]-NPY > NPY 3-36 >> NPY 13-36. The Y1 receptor antagonist, BIBP 3226, blocks NPY inhibition of insulin secretion from, and inhibits 125I-PYY binding to, RIN 5AH cells. Northern blot analysis using a Y1-receptor specific probe shows that NPY Y1 receptors are expressed by RIN 5AH cells. Y5 receptors are not expressed in this cell line. Neuropeptide Y inhibition of insulin secretion is blocked by incubation with pertussis toxin, implying that the effect is via a G-protein (Gi or Go) coupled receptor. Neuropeptide Y inhibits the activation of adenylyl cyclase by isoprenaline in RIN 5AH cell lysates, and the stimulation of cAMP by glucagon-like peptide-1 (7-36) amide (GLP-1). It also blocks insulin secretion stimulated by GLP-1, but not by dibutyryl cyclic AMP. Hence, we suggest that NPY inhibits insulin secretion from RIN 5AH cells via a Y1 receptor linked through Gi to the inhibition of adenylyl cyclase.

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  • NPY binding to its GPCR Y1 causes the activated Giα-subunit to block adenylate cyclase activation, which inhibits the cAMP pathway.

    “NPY binding to its GPCR Y1 causes the activated Giα-subunit to block adenylate cyclase activation, which in turn inhibits the cAMP pathway.121”

    From Pancreatic regulation of glucose homeostasis. (2016) · cites this paper as [121]

    The Discussion (page not specified in our copy) concludes that NPY acts through a Y1 receptor and appears to inhibit adenylyl cyclase through Gi; the paper also reports reduced stimulated cAMP in RIN 5AH cells. It does not establish that the activated Giα subunit specifically causes the inhibition, and its findings are limited to this cell line. (LLM, conf=0.86)

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Metadata

Authors
Morgan, D. G., Kulkarni, R. N., Hurley, J. D., Wang, Z. L., Wang, R. M., Ghatei, M. A., Karlsen, A. E., Bloom, S. R., & Smith, D. M.
Affiliations
  • Hammersmith Hospital (GB)
  • Joslin Diabetes Center (US)
  • Harvard University (US)
ORCID
Venue
Diabetologia
Publisher
Springer Science and Business Media LLC
Published
1998-11-23
Volume
41
Issue
12
Pages
1482-1491
ISSN
  • 0012-186X (ISSN-L)
  • 1432-0428
DOI
10.1007/s001250051095
OpenAlex
W2028903713
Cited by
79
References
44
Citations by year
2024: 1 · 2023: 2 · 2022: 1 · 2021: 3 · 2019: 2 · 2017: 2 · 2016: 4 · 2015: 6 · 2014: 4 · 2013: 1 · 2012: 8
FWCI
3.33
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Diabetologia (publishedVersion)
  • PubMed (publishedVersion)
Funders
Medical Research Council
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords
neuropeptide Y, insulin secretion, Y1 receptor, adenylate cyclase inhibition, insulinoma, BIBP3226, pertussis toxin, G protein-coupled receptors, Gi protein, glucagon-like peptide-1, cyclic AMP, glucose-stimulated insulin secretion
MeSH terms
Adenylyl Cyclase Inhibitors, Insulin Secretion, Cyclic AMP, Adenylyl Cyclases, Animals, Glucagon, Glucose, Insulin, Insulinoma, Iodine Radioisotopes, Isoproterenol, Neuropeptide Y, Pancreatic Neoplasms, Peptide Fragments, Protein Precursors, Swine, Tumor Cells, Cultured, Blotting, Northern, Receptors, Neuropeptide Y, Peptide YY, Rats, Glucagon-Like Peptide 1

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