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Acta Physiologica Congress

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Acta Physiologica 2007; Volume 191, Supplement 658
Joint Meeting of The Slovak Physiological Society, The Physiological Society and The Federation of European Physiological Societies
9/11/2007-9/14/2007
Bratislava, Slovakia


EFFECT OF RESVERATROL ON GLUCOSE- AND SWELLING-INDUCED INSULIN SECRETION
Abstract number: PW05-33

Bacova1 Z., Orecna1 M., Hafko1 R., Strbak1 V.

1Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovakia; [email protected]

Aims: 

Experimental data suggest that resveratrol (3'5'4' trihydroxystilbene, a natural phytoalexin), has a beneficial role in prevention of diabetes and alleviates diabetic complications. Resveratrol substantially restricts glucose-induced insulin secretion from freshly isolated rat pancreatic islets.

Methods: 

To characterize its action, effect of 50 mmol/l resveratrol on 15 mmol/l glucose-, 30% hypotonic medium- and 80 mmol/l ethanol-induced insulin release from freshly isolated pancreatic islets and two rat insulinoma cell lines INS-1 and INS-1E in Ca2+containing medium was compared.

Results: 

Resveratrol significantly decreased glucose-induced insulin release from pancreatic islets and both cell lines. Interestingly, hypotonicity-induced insulin secretion from pancreatic islets was even more pronounced in presence of resveratrol. While hypotonicity alone inhibits insulin release from INS-1E cell line, in the presence of resveratrol hypotonicity induced distinct release of insulin. Resveratrol abolished ethanol-induced insulin release from all tested systems. PDBu (PKC activator) and forskolin (adenylate cyclase activator) partially restored glucose-stimulated insulin secretion in the presence of resveratrol.

Conclusion: 

There is substantial difference in signaling for glucose- and hypotonicity-induced insulin secretion, resveratrol has opposite effect on two pathways. Effect of resveratrol on ethanol-induced insulin secretion resembled that on glucose. It is likely that resveratrol does not involve effect on PKC and cAMP system.

Acknowledgements: 

The work was supported by the project 2/6158/26 of the Grant Agency of Ministry of Education and Slovak Academy of Sciences (VEGA), project APVV 0235-06 and project of CE SAV CENDO.

To cite this abstract, please use the following information:
Acta Physiologica 2007; Volume 191, Supplement 658 :PW05-33

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