Linked Life Data

18815216

Source:http://linkedlifedata.com/resource/pubmed/id/18815216

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2008-11-6
pubmed:abstractText
We previously showed that long-term consumption of a soy protein diet (SoyP) reduces renal damage in obese Zucker (ObeseZ) rats by restoring urinary NO2 and NO3 excretion (UNO2/NO3V), suggesting that nitric oxide (NO) deficiency may contribute to the renal progression observed in this model. In addition, there is compelling evidence that hyperleptinemia produced deleterious effects on the kidney through its interaction with the short leptin receptor (ObRa). This study was designed to evaluate the contribution of the NO/endothelial NO synthase (eNOS) system, renal oxidative stress, and ObRa expression to the renoprotection conferred by the consumption of a SoyP in ObeseZ rats. Ten lean and ten male ObeseZ rats were included. One-half of each group was fed with a 20% SoyP and the other half with a 20% casein protein diet (CasP) over the course of 160 days. eNOS protein levels and phosphorylation, renal lipoperoxidation (rLPO), and antioxidant enzyme activity were assessed. In addition, renal ObRa, TGF-beta, and kidney injury molecule (Kim-1) mRNA levels, as well as urinary Kim-1 levels, were measured. Renal injury observed in ObeseZ rats fed with CasP was not associated with changes in eNOS expression or phosphorylation. However, this group did present with increased rLPO, reduced catalase activity, and upregulation of ObRa, TGF-beta1, and Kim-1. In contrast, ObeseZ rats fed with a SoyP exhibited a reduction in NOS-Thr495 phosphorylation and rLPO, as well as an enhanced catalase activity. These findings were associated with a significant reduction of ObRa, TGF-beta1, and Kim-1 mRNA levels and urinary Kim-1 protein. Our results show that renoprotection by SoyP in ObeseZ rats is in part mediated by increased NO availability secondary to a reduction in eNOS-T495 phosphorylation and oxidative stress, together with a significant reduction in ObRa and TGF-beta expression.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1931-857X
pubmed:author
pubmed:issnType
Print
pubmed:volume
295
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
F1574-82
pubmed:dateRevised
2011-4-28
pubmed:meshHeading
pubmed-meshheading:18815216-Administration, Oral, pubmed-meshheading:18815216-Animals, pubmed-meshheading:18815216-Antioxidants, pubmed-meshheading:18815216-Blotting, Western, pubmed-meshheading:18815216-Caseins, pubmed-meshheading:18815216-Cell Adhesion Molecules, pubmed-meshheading:18815216-Dietary Proteins, pubmed-meshheading:18815216-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:18815216-Gene Expression, pubmed-meshheading:18815216-Kidney, pubmed-meshheading:18815216-Kidney Diseases, pubmed-meshheading:18815216-Kidney Glomerulus, pubmed-meshheading:18815216-Leptin, pubmed-meshheading:18815216-Lipid Peroxidation, pubmed-meshheading:18815216-Male, pubmed-meshheading:18815216-Nitric Oxide Synthase Type III, pubmed-meshheading:18815216-Obesity, pubmed-meshheading:18815216-Oxidative Stress, pubmed-meshheading:18815216-Phosphorylation, pubmed-meshheading:18815216-Rats, pubmed-meshheading:18815216-Rats, Zucker, pubmed-meshheading:18815216-Receptors, Leptin, pubmed-meshheading:18815216-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:18815216-Soybean Proteins, pubmed-meshheading:18815216-Transforming Growth Factor beta
pubmed:year
2008
pubmed:articleTitle
Renoprotective mechanisms of soy protein intake in the obese Zucker rat.
pubmed:affiliation
Molecular Physiology Unit, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Mexico.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't