Curcumin Exhibits Liver and Kidney Protection in Fructose-Induced Rat Model of Metabolic Syndrome

Excess fructose consumption is suggested to be a potential risk factor for metabolic syndrome with hepatic steatosis and renal injury [1 – 2]. Curcumin, a natural plant phenolic compound, exerts beneficial effects on human health. The present study further confirmed that curcumin revised fructose-induced metabolic syndrome in rats. Curcumin was found to significantly reduce hepatic expression and activity of protein tyrosine phosphatase 1B (PTP1B) associated with its improvement of insulin and leptin signal pathway and sensitivity in fructose-fed rats. Subsequently, it up-regulated hepatic expression of peroxisome proliferator-activated receptor α (PPARα) in this model, resulting in its reduction of lipid accumulation and hepatic steatosis. Moreover, curcumin increased nitric oxide (NO) production as well as inhibited activation of the janus kinase 2/signal transducer and activator of transcription 3 (JAK2-STAT3) pathway and up-regulation of suppressor of cytokine signaling 3 (SOCS3) and transforming growth factor β1 (TGF-β1) in the kidney of fructose-fed rats, showing its amelioration of renal endothelial dysfunction. These results may provide the evidence for the potential use of a functional food ingredient curcumin to recover hepatic steatosis and renal damage driven by high fructose intake.

Acknowledgements: This study is supported by grants from National Natural Science Foundation of China (NSFC 81025025) and Program for Changjiang Scholars and Innovative Research Team in University (IRT1020). References: [1] Ouyang X, et al. (2008)J Hepatol, 48: 993 – 999. [2] Johnson RJ, et al. (2007) Am J Clin Nutr, 86: 899 – 906.