Cocoa flavonoid epicatechin protects pancreatic beta cell viability and function against oxidative stress. Issue 3 (1st October 2013)

• Record Type: Journal Article
• Authors: Martín, María Ángeles; Fernández‐Millán, Elisa; Ramos, Sonia; Bravo, Laura; Goya, Luis
• Is Part Of: Molecular nutrition & food research. Volume 58:Issue 3(2014:Mar.)
• Page Start: 447
• Page End: 456
• Publication Date: 2013-10-01
• Subjects: Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201300291
• Languages: English
• ISSNs: 1613-4125

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2087-sec-0010" sec-type="section"> <title>Scope</title> <p>Diabetes mellitus is associated with reductions in glutathione, supporting the critical role of oxidative stress in its pathogenesis. Antioxidant food components such as flavonoids have a protective role against oxidative stress‐induced degenerative and age‐related diseases. Flavonoids such as epicatechin (EC) constitute an important part of the human diet; they can be found in green tea, grapes, and cocoa and possess multiple biological activities. This study investigates the chemo‐protective effect of EC against oxidative stress induced by <italic>tert</italic>‐butylhydroperoxide (<italic>t</italic>‐BOOH) on Ins‐1E pancreatic beta cells.</p> </sec> <sec id="mnfr2087-sec-0020" sec-type="section"> <title>Methods and results</title> <p>Cell viability, oxidative status, phosphorylated Jun kinase (p‐JNK) expression, and insulin secretion were evaluated. Ins‐1E cells treatment with 5–20 μM EC for 20 h evoked no cell damage and enhanced antioxidant enzymes and insulin secretion. Addition of 50 μM <italic>t</italic>‐BOOH for 2 h induced reactive oxygen species, p‐JNK, and carbonyl groups and decreased GSH and insulin secretion. Pretreatment of cells with EC prevented the <italic>t</italic>‐BOOH‐induced reactive oxygen species, carbonyl groups, p‐JNK expression and cell death, and recovered insulin secretion.</p> </sec> <sec id="mnfr2087-sec-0030" sec-type="section"> <title>Conclusion</title> <p>Ins‐1E cells treated with EC showed a remarkable recovery of cell viability and insulin secretion damaged by <italic>t</italic>‐BOOH, indicating that integrity of secreting and surviving machineries in the EC‐treated cells was notably protected against the oxidative insult.</p> </sec> </abstract>