RGD Reference Report - Disorder of fatty acid metabolism in the kidney of PAN-induced nephrotic rats. - Rat Genome Database

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Disorder of fatty acid metabolism in the kidney of PAN-induced nephrotic rats.

Authors: Muroya, Y  Ito, O  Rong, R  Takashima, K  Ito, D  Cao, P  Nakamura, Y  Joh, K  Kohzuki, M 
Citation: Muroya Y, etal., Am J Physiol Renal Physiol. 2012 Oct;303(7):F1070-9. doi: 10.1152/ajprenal.00365.2011. Epub 2012 Aug 8.
RGD ID: 7242024
Pubmed: PMID:22874759   (View Abstract at PubMed)
DOI: DOI:10.1152/ajprenal.00365.2011   (Journal Full-text)

Proteinuria is considered to play an essential role in the progression of tubulointerstitial damage, which causes end-stage renal disease. Fatty acid-binding albumins are filtered through glomeruli and reabsorbed into proximal tubular epithelial cells (PTECs). However, the role of fatty acid metabolism associated with albuminuria in the development of tubulointerstitial damage remains unclear. Thus, the present study was designed to determine the changes of fatty acid metabolism in the nephrotic kidney. To induce nephrotic syndrome, Sprague-Dawley rats (SDRs) and Nagase analbuminemic rats (NARs) with inherited hypoalbuminemia were treated with a single injection of puromycin aminonucleoside (PAN). In SDRs, PAN treatment induced massive proteinuria and albuminuria and caused tubular damage, apoptosis, and lipid accumulation in PTECs. Among the enzymes of fatty acid metabolism, expressions of medium-chain acyl-CoA dehydrogenase (MCAD) and cytochrome P-450 (CYP)4A significantly decreased in PTECs of PAN-treated SDRs. Expressions of peroxisome proliferator-activated receptor (PPAR)-gamma coactivator (PGC)-1alpha and estrogen-related receptor (ERR)alpha also significantly decreased, without changes in the expression of PPAR-alpha. In NARs, PAN treatment induced proteinuria but not albuminuria and did not cause tubular damage, apoptosis, or lipid accumulation. Expressions of MCAD, PGC-1alpha, or ERRalpha did not change in the kidney cortex of PAN-treated NARs, but the expression of CYP4A significantly decreased. These results indicate that massive albuminuria causes tubular damage and lipid accumulation with the reduction of MCAD, CYP4A, PGC-1alpha, and ERRalpha in PTECs.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
nephrotic syndrome  ISOPpargc1a (Rattus norvegicus)7242024; 7242024protein:decreased expression:kidney cortex (rat)RGD 
nephrotic syndrome  IEP 7242024protein:decreased expression:kidney cortex (rat)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ppargc1a  (PPARG coactivator 1 alpha)

Genes (Mus musculus)
Ppargc1a  (peroxisome proliferative activated receptor, gamma, coactivator 1 alpha)

Genes (Homo sapiens)
PPARGC1A  (PPARG coactivator 1 alpha)


Additional Information