Background and Objectives: The excess consumption of fructose in the diet may cause metabolic syndrome, which is associated with an increased risk of kidney disease. There is limited data on probiotic treatment in high-fructose-induced metabolic syndrome. The present study aims to investigate whether the supplementation of Lactobacillus plantarum (L. plantarum) and Lactobacillus helveticus (L. helveticus) could provide an improving effect on the renal insulin signaling effectors, inflammatory parameters, and glucose transporters in fructose-fed rats. Materials and Methods: The model of metabolic syndrome in male Wistar rats was produced by fructose, which was given as 20% solution in drinking water for 15 weeks. L. plantarum and L. helveticus supplementations were given by gastric gavage from 10 to 15 weeks of age. Results: High-fructose consumption in rats reduced renal protein expressions of insulin receptor substrate (IRS)-1, protein kinase B (AKT), and endothelial nitric oxide synthase (eNOS), which were improved by L. plantarum and partially by L. helveticus supplementations. Dietary fructose-induced elevations in renal tissue levels of tumor necrosis factor α (TNF-α), interleukin (IL)-1β, IL-6, and IL-10, as well as expression of IL-6 mRNA, were attenuated, especially in L. plantarum treated rats. The increased renal expression of sodium-glucose cotransporter-2 (SGLT2), but not that of glucose transporter type-5 (GLUT5), was suppressed by the treatment with L. plantarum. Conclusion: Suppression in insulin signaling pathway together with the induction of inflammatory markers and upregulation of SGLT2 in fructose-fed rats were improved by L. plantarum supplementation. These findings may offer a new approach to the management of renal dysregulation induced by dietary high-fructose.
High dietary fructose intake causes a metabolic disorder and augments the risk of chronic kidney disease most likely due to oxidative stress. Probiotics could have antioxidant, antiinflammatory and immunoregulatory properties. The present study examined the influence of Lactobacillus helveticus and Lactobacillus plantarum supplementation on dietary fructose-induced metabolic changes and renal antioxidant/oxidant status of rats. Male Wistar rats were divided into four groups as follows: control; fructose; fructose plus L. helveticus; fructose plus L. plantarum. Fructose was given to the rats as a 20% solution in drinking water for 15 weeks. The probiotic supplementation was applied by gastric gavage once a day for six weeks. Several metabolic parameters in the plasma, gene and protein expressions of the main antioxidant enzymes in renal tissues of rats were measured. Dietary fructose-induced elevations in plasma insulin, triglyceride, VLDL, creatinine as well as renal urea levels were alleviated after treatment with L. helveticus and L. plantarum. Moreover, L. helveticus and L. plantarum supplementation recovered the changes in renal protein expression level of SOD1, SOD2 and CAT. In conclusion, supplementation with L. helveticus and L. plantarum has an improving effect on specific metabolic parameters and renal antioxidative enzymes in a fructose-induced metabolic disorder.
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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