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cAMP-PKA dependent ERK1/2 activation is necessary for vanillic acid potentiated glucose-stimulated insulin secretion in pancreatic β-cells.

Mahendra, V. P. and Devendra, J. Haware and Ravi, Kumar (2019) cAMP-PKA dependent ERK1/2 activation is necessary for vanillic acid potentiated glucose-stimulated insulin secretion in pancreatic β-cells. Journal of Functional Foods, 56. pp. 110-118. ISSN 1756-4646

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Abstract

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 cellline 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.

Item Type: Article
Uncontrolled Keywords: Vanillic acid PKA GSIS ERK1/2 Pancreatic β-cells cAMP
Subjects: 500 Natural Sciences and Mathematics > 10 Plants
600 Technology > 01 Medical sciences > 04 Diabetes Mellitus
Divisions: Food Safety Analytical Quality Control Lab
Molecular Nutrition
Depositing User: Food Sci. & Technol. Information Services
Date Deposited: 03 Jun 2019 06:23
Last Modified: 03 Jun 2019 06:23
URI: http://ir.cftri.com/id/eprint/14118

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