METODO DI BELLA > PRINCIPI ATTIVI > Melatonina > Transcripts of calcium/calmodulin-dependent kinases are changed after forskolin- or IBMX-induced insulin secretion due to melatonin treatment of rat insulinoma beta-cells (INS-1).

 
Transcripts of calcium/calmodulin-dependent kinases are changed after forskolin- or IBMX-induced insulin secretion due to melatonin treatment of rat insulinoma beta-cells (INS-1). di Bazwinsky-Wutschke I, Mühlbauer E, Wolgast S, Peschke E.
 
 
Data: 06/05/2011
Tipologia: DOCUMENTAZIONE SCIENTIFICA
Lingua: Inglese
Anno: 2009
Fonte: Horm Metab Res. 2009 Nov;41(11):805-13.
 
 
Descrizione:

The objective of the present study was to examine the effects of melatonin on transcripts of isoforms of calcium/calmodulin-dependent protein kinases in rat insulinoma beta-cells INS-1. Investigations show that calcium/calmodulin-dependent kinase IV and calcium/calmodulin-dependent kinase 2d are expressed in human and rat pancreatic islets and INS-1 cells. By application of either forskolin or 3-isobutyl-1-methylxanthine for 6 hours, calcium spiking was evoked and the release of insulin was increased. The expression of the calcium/calmodulin-dependent kinase IV and calcium/calmodulin-dependent kinase 2d transcripts was significantly increased due to forskolin or 3-isobutyl-1-methylxanthine. Acute melatonin treatment (6 h) in the presence of either forskolin or 3-isobutyl-1-methylxanthine caused a significant decrease in insulin release and induced significant downregulation of calcium/calmodulin-dependent kinase IV and calcium/calmodulin-dependent kinase 2d transcripts in INS-1 batch cultures. The attenuating effect of melatonin on transcripts could be almost completely reversed by preincubation with the melatonin receptor antagonist luzindole. Thus, the insulin-inhibiting effect of melatonin in INS-1 cells is associated with significant changes in transcripts of calcium-signaling components suggesting that melatonin influences gene expression of components, which are known to be involved in insulin secretion or insulin gene expression.

 
 
 
 

 

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