Cited by 73Neuropeptides and Animal PhysiologyThyroid Disorders and TreatmentsPancreatic function and diabetes

Expression of glucagon‐like peptide 1 receptor in a murine C cell line Regulation of calcitonin gene by glucagon‐like peptide 1

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Lamari, Y., Boissard, C., Moukhtar, M.S., Jullienne, A., Rosselin, G., Garel, J.-M.·1996·FEBS Letters

Abstract

We have characterized, by RT‐PCR amplification using specific primers, the presence of glucagon‐like peptide‐1 (GLP‐1) receptor mRNA in CA‐77 cells, a C cell line derived from a rat medullary thyroid carcinoma. Down‐regulation of the GLP‐1 receptor mRNA was observed after exposure of CA‐77 C cells with GLP‐1 (7–37). Increased secretion of both calcitonin gene‐related peptide (CGRP) and calcitonin (CT) occurred after treatment with GLP‐1 (7–37) associated with elevated steady‐state levels of CGRP and CT mRNA. GLP‐1 (7–37) increased cAMP formation in CA‐77 cells in a dose‐dependent manner; exendin (9–39), a GLP‐1 receptor antagonist, inhibited cAMP production. The GLP‐1 peptide which is produced by intestinal cells could be involved in the control of CT secretion through an entero‐thyroidal axis implying GLP‐1 receptor and increased CT gene expression.

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Crossref · 10.1016/0014-5793(96)00895-2

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  • GLP-1R is expressed in thyroid C cells and GLP-1 directly stimulates secretion of calcitonin, which is a potent inhibitor of bone resorption in osteoclasts; GLP-1 may contribute to nutrient-mediated reduction in bone resorption.

    “Since GLP-1R is expressed in thyroid C cells and GLP-1 directly stimulates the secretion of calcitonin, which is a potent inhibitor of bone resorption in osteoclasts, GLP-1 may contribute to the nutrient-mediated reduction in bone resorption.369,370”

    From Glucagon-like peptide-1 receptor: mechanisms and advances in therapy (2024) · cites this paper as [370]

    The Discussion and section 3.2.2 report GLP-1 receptor mRNA in a rat thyroid C-cell line and increased calcitonin secretion after GLP-1 treatment. The Discussion suggests intestinal GLP-1 could help control calcitonin secretion, but the paper does not address osteoclasts or show a nutrient-mediated reduction in bone resorption; its experiments were in a cell line, not thyroid C cells in vivo. Page numbers are unavailable in our copy. (LLM, conf=0.86)

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  • It is plausible that calcitonin plays a role in alterations in bone metabolism observed in GLP-1R-treated animals.

    “Considering the expression of the GLP-1R in thyroid C cells and the ability of GLP-1 to stimulate calcitonin secretion through a cAMP-mediated mechanism in vitro, it is plausible that calcitonin plays a role in the alterations in bone metabolism observed in GLP-1R-treated animals.369,370”

    From Glucagon-like peptide-1 receptor: mechanisms and advances in therapy (2024) · cites this paper as [370]

    The Results and Discussion report GLP-1 receptor expression in CA-77 C cells, increased calcitonin secretion after GLP-1 treatment, and increased cAMP production. These in vitro findings provide a basis for the citing authors’ proposed explanation, but the paper does not examine bone metabolism or establish a role for calcitonin in the alterations observed in GLP-1R-treated animals. (LLM, conf=0.84)

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References 25 · Cited by 73

Research works printed but not linked: 5

  1. [8]8. Thomas, P.S. (1980) Proc. Natl. Acad. Sci. USA 77, 5201 5205.
  2. [9]9. Thorens, B. (1992) Proc. Natl. Acad. Sci. USA 89, 8641-8645.
  3. [17]17. Laburthe, M., Rousset, M., Boissard, C., Chevalier, G., Zwei- baum, A. and Rosselin, G. (1978) Proc. Natl. Acad. Sci. USA 75, 2772 2775.
  4. [18]18. Marie, J.C., Boissard, C., Skoglund, G., Rosselin, G. and Breant, B. (1996) Endocrinology 138, in press.
  5. [24]24. Drucker, D.J., Philippe, J., Mojsov, S., Chick, W.L. and Habe- ner, J.F. (1987) Proc. Natl. Acad. Sci. USA 84, 3434-3438.

Authors
Lamari, Y., Boissard, C., Moukhtar, M. S., Jullienne, A., Rosselin, G., & Garel, J.-M.
Affiliations
  • Université Pierre-et-Marie-Curie (FR)
  • Inserm (FR)
Venue
FEBS Letters
Publisher
Wiley
Published
1996-09-16
Volume
393
Issue
2-3
Pages
248-252
ISSN
  • 0014-5793 (ISSN-L)
  • 1873-3468
OpenAlex
W2079440907
Cited by
73
References
25
Citations by year
2026: 1 · 2025: 4 · 2024: 5 · 2023: 2 · 2022: 1 · 2019: 1 · 2018: 3 · 2017: 6 · 2016: 3 · 2015: 7 · 2014: 6 · 2013: 6 · 2012: 4
FWCI
0.41
Type
journal article
Language
en
Open access
Locations
  • FEBS Letters (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • University of Miami
  • Mayo Foundation for Medical Education and Research
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
GLP-1 receptor, calcitonin gene, calcitonin, calcitonin gene-related peptide, C cells, medullary thyroid carcinoma, exendin-9-39, cAMP signaling, gene expression regulation
MeSH terms
Glucagon-Like Peptide-1 Receptor, Animals, Base Sequence, Calcitonin, Cell Line, Glucagon-Like Peptides, Glucagon, Kinetics, Molecular Sequence Data, Peptide Fragments, Peptides, RNA, Messenger, Thyroid Neoplasms, Transcription, Genetic, Tumor Cells, Cultured, Oligonucleotide Probes, Calcitonin Gene-Related Peptide, Gene Expression Regulation, Neoplastic, Polymerase Chain Reaction, DNA Primers, Receptors, Glucagon, Rats, Glucagon-Like Peptide 1

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