Curcumin protects against fructose-induced podocyte insulin signaling impairment through up-regulation of miR-206.
Mol Nutr Food Res. 2015 Sep 23. Epub 2015 Sep 23. PMID: 26395192
SCOPE: Fructose consumption can induce insulin resistance and metabolic syndrome, which are associated with glomerular podocyte dysfunction and proteinuria. This study investigated whether fructose caused insulin signaling impairment in podocyte dysfunction and injury, and whether curcumin reduced these disturbances.
METHODS AND RESULTS: Rats were exposed to 10% fructose for 6 weeks and then orally co-treated with curcumin for next 6 weeks. Metabolic syndrome, podocyte injury, microRNA (miRNA) expression and insulin signaling were evaluated. Curcumin significantly alleviated fructose-induced podocyte injury and proteinuria, miR-206 low-expression, protein tyrosine phosphatase-1B (PTP1B) overexpression, as well as down-regulation of insulin receptor, insulin receptor substrate-1, caveolin-1, protein kinase B, and extracellular signal-regulated kinases 1 and 2 phosphorylation in kidney cortex or glomeruli of fructose-fed rats. These effects were further confirmed in cultured differentiated podocytes exposed to 5 mM fructose in the presence or absence of curcumin, PTP1B siRNA, lentivirus-mediated PTP1B recombinant overexpression, miR-206 mimic or miR-206 inhibitor transfection, showing that miR-206 up-regulation may contribute to improve insulin signaling through regulating PTP1B expression.
CONCLUSION: Curcumin may activate miR-206 expression to down-regulate PTP1B, and then improve insulin signaling, protect against fructose-induced glomerular podocyte injury and proteinuria, which may provide new evidence regarding curcumin's effects on fructose-associated podocyte injury. This article is protected by copyright. All rights reserved.