Renoprotective mechanisms of soy protein (SP) in obese Zucker rat (OZ).

Abstract

We showed that SoyP feeding reduces renal damage in OZ that was associated with restoration of NO2/NO3 excretion and reduction of membrane endothelial nitric oxide synthase (eNOS) and caveolin. It has been shown that eNOS activity is regulated by its phosphorylation state. In addition, exists evidences that leptin may exert kidney deleterious actions through leptin short receptor (ObRa) activation, that stimulates TGFβ and collagen overexpression, as well as ROS formation. In this study we evaluated 1) If SoyP changes eNOS-T495 phosphorylated amount in OZ, 2) if renal injury is associated with ObRa, TGFβ, and renal kidney injury molecule (KIM1) up-regulation, and 3) if SoyP modifies these genes expression and lipoperoxidation levels. Ten male Lean Zucker (ZL) and ten OZ rats were included. One half was fed with 20% SoyP and the other with 20% casein (Cas) for 160 days. eNOS-T495 protein and lipoperoxidation levels, as well as Ob-Ra, TGFβ and KIM-1 renal cortex mRNA levels were evaluated. SoyP reduced eNOS-T495 and lipoperoxidation levels. OZ fed with casein had Ob-Ra, TGFβ, and KIM-1 up-regulation, in contrast SoyP feeding normalized Ob-Ra and significantly reduced TGFβ and KIM-1 mRNA levels. Nitric oxide restoration in OZ fed with SoyP could in part result from reduction of eNOS-T495 and lipoperoxidation. Our results also suggest that the renoprotective of SoyP seems to be mediated by reduction of Ob-Ra and TGFβ mRNA levels.