Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 191, Issue 2, Pages 157-166Publisher
ELSEVIER SCI IRELAND LTD
DOI: 10.1016/S0303-7207(02)00064-3
Keywords
melatonin 1a receptor; glucagon-like peptide-1; insulin; pancreatic beta cell
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Funding
- NIDDK NIH HHS [DK-30834] Funding Source: Medline
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Melatonin receptors are expressed within the pancreatic islets of Langerhans, and melatonin induces a direct effect oil insulin secretion ex-vivo. Here, we report the endogenous expression of the melatonin Mel la receptor in the INS-1 pancreatic 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 la receptor, and may represent the first evidence of a specific physiological role for melatonin-induced sensitization. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
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