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Cocoa flavonoid epicatechin protects pancreatic beta cell viability and function against oxidative stress

Authors

  • María Ángeles Martín,

    1. Departamento de Metabolismo y Nutrición; Instituto de Ciencia y Tecnología de Alimentos y Nutrición (ICTAN – CSIC), Madrid, Spain
    2. Centro de Investigación Biomédica en red de Diabetes y Enfermedades Metabólicas Asociadas (ISCIII), Madrid, Spain
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  • Elisa Fernández-Millán,

    1. Centro de Investigación Biomédica en red de Diabetes y Enfermedades Metabólicas Asociadas (ISCIII), Madrid, Spain
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  • Sonia Ramos,

    1. Departamento de Metabolismo y Nutrición; Instituto de Ciencia y Tecnología de Alimentos y Nutrición (ICTAN – CSIC), Madrid, Spain
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  • Laura Bravo,

    1. Departamento de Metabolismo y Nutrición; Instituto de Ciencia y Tecnología de Alimentos y Nutrición (ICTAN – CSIC), Madrid, Spain
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  • Luis Goya

    Corresponding author
    1. Departamento de Metabolismo y Nutrición; Instituto de Ciencia y Tecnología de Alimentos y Nutrición (ICTAN – CSIC), Madrid, Spain
    • Correspondence: Dr. Luis Goya, Departamento de Metabolismo y Nutrición, Instituto de Ciencia y Tecnología de Alimentos y Nutrición (ICTAN – CSIC), José Antonio Novais, 10, 28040 Madrid, Spain

      E-mail: luisgoya@ictan.csic.es

      Fax: +34-91-549-36-27

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Abstract

Scope

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 tert-butylhydroperoxide (t-BOOH) on Ins-1E pancreatic beta cells.

Methods and results

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 t-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 t-BOOH-induced reactive oxygen species, carbonyl groups, p-JNK expression and cell death, and recovered insulin secretion.

Conclusion

Ins-1E cells treated with EC showed a remarkable recovery of cell viability and insulin secretion damaged by t-BOOH, indicating that integrity of secreting and surviving machineries in the EC-treated cells was notably protected against the oxidative insult.

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