Compound K protects MIN6N8 pancreatic β-cells against palmitate-induced apoptosis through modulating SAPK/JNK activation

Authors

  • Kyong Kim,

    1. Functional Food Technology Research Group, Research Division for Emerging Innovative Technology, Korea Food Research Institute, 516 Baekhyun-dong, Bundang-gu, Songnam-si, Kyonggi-do 463-746, Republic of Korea
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  • Dong-Hyun Kim,

    1. College of Pharmacy, Kyunghee University, 1 Heogi-dong, Dongdaemun-gu, Seoul 130-701, Republic of Korea
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  • Young Hye Kim

    Corresponding author
    1. Functional Food Technology Research Group, Research Division for Emerging Innovative Technology, Korea Food Research Institute, 516 Baekhyun-dong, Bundang-gu, Songnam-si, Kyonggi-do 463-746, Republic of Korea
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email khyey@kfri.re.kr

Abstract

Chronic elevation of NEFAs (non-esterified fatty acids) due to insulin resistance and obesity has been shown to be associated with increased β-cell apoptosis and with the aetiology of the reduced β-cell mass of Type 2 diabetes. SAPK (stress-activated protein kinase)/JNK (c-Jun N-terminal kinase) have been implicated in the control of apoptosis. C-K [compound K; 20-O-β-d-glucopyranosyl-20(S)-protopanaxadiol] is the main intestinal bacterial metabolite of protopanaxadiol ginsenosides. Currently, little is known about the effects of C-K on β-cells with the presence of NEFAs. The aim of the present study was to investigate the in vitro protective effect of C-K on MIN6N8 mouse insulinoma β-cells against NEFA-induced apoptosis, as well as the modulating effect on SAPK/JNK activation. Our results have shown that C-K inhibited the palmitate-induced apoptosis through modulating SAPK/JNK activation. We conclude that C-K protects against β-cell death and that, by anti-apoptotic activity, C-K may contribute to the previously reported anti-diabetic actions of ginseng.

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