Kefir protects the liver against high fructose corn syrup induced phosphodiesterase hyperactivity

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Abstract
Objectives: Phosphodiesterases (PDEs) mediate several physiological activities, and alterations in PDE expressions might cause conflicts between functional and clinical effects. This study clarifies the eventual relationship between the hepatic insulin resistance-associated signaling elements and PDEs together with inflammatory markers and investigates the role of kefir in the treatment. Methods: Male Wistar rats were grouped as Control, Kefir, HFCS (high-fructose corn syrup), and HFCS + Kefir. Daily HFCS (20% w/v) and kefir (1 mL/100 g weight) were given for 8-weeks. Hepatic expressions of PDE isoforms and insulin signaling elements were determined with qPCR and Western blot. The changes in hepatic phospholipase A2 (cPLA2) and insulin-like growth factor 1 receptor-α (IGF-1Rα) were investigated histologically. Results: HFCS upregulated hepatic PDEs while repressed primary insulin signaling elements at gene and protein levels. It also augmented cPLA2 and IGF-1Rα expression. Kefir suppressed the PDEs and normalized the insulin signaling, and down-regulated cPLA2 and IGF-1Rα in the liver of HFCS-fed rats. Conclusions: The disruption of the insulin signaling pathway and activation of PDEs were negatively correlated in liver tissues of the HFCS-fed rats. Kefir treatment achieved a remarkable improvement in HFCS-dependent modifications, and it could be an excellent functional food against HFCS-induced insulin resistance, PDE hyperactivity, and inflammation.

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