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

Chronic elevation of NEFAs (non-esterified fatty acids) due to insulin resistance and obesity has been shown to be associated with increased beta-cell apoptosis and with the aetiology of the reduced beta-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-beta-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 beta-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 beta-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 beta-cell death and that, by anti-apoptotic activity, C-K may contribute to the previously reported anti-diabetic actions of ginseng.