cAMP-PKA dependent ERK1/2 activation is necessary for vanillic acid potentiated glucose-stimulated insulin secretion in pancreatic β-cells
[Display omitted] •Vanillic acid is shown to potentiate GSIS in pancreatic β-cells.•Vanillic acid enhances cAMP level that activates PKA in pancreatic β-cells.•Vanillic acid potentiated GSIS is dependent on ERK1/2 activation. Vanillic acid (VA), a dietary phenolic compound is generally studied for i...
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Veröffentlicht in: | Journal of functional foods 2019-05, Vol.56, p.110-118 |
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Sprache: | eng |
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•Vanillic acid is shown to potentiate GSIS in pancreatic β-cells.•Vanillic acid enhances cAMP level that activates PKA in pancreatic β-cells.•Vanillic acid potentiated GSIS is dependent on ERK1/2 activation.
Vanillic acid (VA), a dietary phenolic compound is generally studied for its anti-oxidative and anti-inflammatory effects. However, the effect of VA on insulin secretion and its mechanism of action has never been explored. In this study, we report that VA augments glucose-stimulated insulin secretion (GSIS) in both insulin-secreting cell-line INS-1 and isolated rat pancreatic islets. Potentiation of GSIS is accompanied by a concurrent increase in 3′,5′-cyclic adenosine monophosphate (cAMP) and activation of protein kinase A (PKA) in INS-1 and rat islets. The activated cAMP-PKA pathway, in turn, phosphorylates extracellular signal-regulated kinases 1/2 (ERK1/2) in INS-1 cells. Pharmacological intervention with PKA and ERK1/2 inhibitors revealed that VA potentiated GSIS is primarily dependent on PKA mediated ERK1/2 activity. These findings demonstrated that VA directly acts on insulin-secreting pancreatic β-cells to exert its insulinotropic effect thereby providing a novel role of VA in the regulation of insulin secretion. |
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ISSN: | 1756-4646 2214-9414 |
DOI: | 10.1016/j.jff.2019.02.047 |