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Cited by 122Pancreatic function and diabetesCircadian rhythm and melatoninDiabetes Treatment and Management

The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.

Identification and functional characterization of melatonin Mel 1a receptors in pancreatic β cells: potential role in incretin-mediated cell function by sensitization of cAMP signaling

Kemp, Daniel M, Ubeda, Mariano, Habener, Joel F·2002·Molecular and Cellular Endocrinology
DOI 10.1016/s0303-7207(02)00064-3
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Abstract

Melatonin receptors are expressed within the pancreatic islets of Langerhans, and melatonin induces a direct effect on insulin secretion ex-vivo. Here, we report the endogenous expression of the melatonin Mel 1a receptor in the INS-1 pancreatic beta cell line. Pharmacological characterization of the receptor using a CRE-luciferase reporter gene demonstrated its functional activity in INS-1 cells, displaying the characteristic signaling properties of the G(i/o) coupled receptor. Acute melatonin treatment of INS-1 cells in the presence of either forskolin or the incretin hormone glucagon-like peptide 1 (GLP-1) caused an attenuation of the responses in insulin secretion, insulin promoter activity, and CRE mediated gene expression, consistent with its effects in inhibiting cAMP mediated signal transduction. However, prolonged exposure (12 h) of INS-1 cells to melatonin treatment resulted in a sensitization of cAMP mediated responses to forskolin and GLP-1. Insulin secretion, insulin promoter activity and CRE mediated gene expression levels were augmented compared with responses without melatonin pre-treatment in INS-1 cells. In isolated rat islets, insulin secretion was enhanced following melatonin pre-treatment both in the absence and presence of GLP-1 or forskolin. This phenomenon reflects observations reported in other cell types expressing the melatonin Mel 1a receptor, and may represent the first evidence of a specific physiological role for melatonin-induced sensitization.

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Metadata

Authors
Kemp, D. M., Ubeda, M., & Habener, J. F.
Affiliations
Howard Hughes Medical Institute (US)
Corresponding author
Habener, Joel F
Venue
Molecular and Cellular Endocrinology
Publisher
Elsevier BV
Published
2002-06
Volume
191
Issue
2
Pages
157-166
ISSN
0303-7207 (ISSN-L)
DOI
10.1016/s0303-7207(02)00064-3
OpenAlex
W2064385910
Cited by
122
References
40
Citations by year
2026: 1 · 2025: 4 · 2024: 4 · 2023: 5 · 2022: 3 · 2021: 7 · 2020: 1 · 2019: 6 · 2018: 9 · 2017: 2 · 2016: 7 · 2015: 13 · 2014: 9 · 2013: 10 · 2012: 2
FWCI
2.23
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Molecular and Cellular Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (DK 30834, R01DK030834)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords
melatonin, pancreatic beta cells, insulin secretion, incretins, glucagon-like peptide-1, cAMP signaling, forskolin, G protein-coupled receptors, INS-1 cells, pancreatic islets
MeSH terms
Cyclic AMP, Animals, Cell Line, Circadian Rhythm, Glucagon-Like Peptides, Glucagon, Islets of Langerhans, Melatonin, Peptide Fragments, Protein Precursors, Receptors, Cell Surface, Second Messenger Systems, Receptors, Cytoplasmic and Nuclear, Receptors, Melatonin, Rats, Glucagon-Like Peptide 1

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