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• W2121378766 abstract "Abstract: The effects of melatonin in mammalian cells are exerted via specific receptors or are related to its free radical scavenging activity. It has previously been reported that melatonin inhibits insulin secretion in the pancreatic islets of the rat and in rat insulinoma INS1 cells via G i ‐protein‐coupled MT1 receptors and the cyclic adenosine 3′,5′‐monophosphate pathway. However, the inositol‐1,4,5‐trisphosphate (IP 3 ) pathway is involved in the insulin secretory response as well, and the melatonin signal may play a part in its regulation. This paper addresses the involvement of the second messengers IP 3 and intracellular Ca 2+ ([Ca 2+ ] i ) in the signalling cascade of melatonin in the rat insulinoma INS1 cell, a model for the pancreatic β ‐cell. For this purpose melatonin at concentrations ranging from 1 to 100 nmol/L, carbachol and the nonselective melatonin receptor antagonist luzindole were used to stimulate INS1 cell batches, followed by an IP 3 ‐mass assay and Ca 2+ imaging. Molecular biological studies relating to the mRNA of IP 3 receptor (IP 3 R) subtypes and their relative abundance in INS1 cells showed expression of IP 3 R‐1, IP 3 R‐2 and IP 3 R‐3 mRNA. In conclusion, we found that in rat insulinoma INS1 cells there is a dose‐dependent stimulation of IP 3 release by melatonin, which is accompanied by a likewise transient increase in [Ca 2+ ] i concentrations. The melatonin effect observed mimics carbachol action. It can be abolished by 30 μ mol/L luzindole and is sustained in Ca 2+ ‐free medium, suggesting a mechanism that includes the depletion of Ca 2+ from intracellular stores." @default.
• W2121378766 created "2016-06-24" @default.
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• W2121378766 date "2005-06-15" @default.
• W2121378766 modified "2023-10-11" @default.
• W2121378766 title "Melatonin stimulates inositol-1,4,5-trisphosphate and Ca2+ release from INS1 insulinoma cells" @default.
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• W2121378766 doi "https://doi.org/10.1111/j.1600-079x.2005.00253.x" @default.
• W2121378766 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16150114" @default.
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