title: Dietary conjugated linoleic acid reduces PGE2 release and interstitial injury in rat polycystic kidney disease.
abstract: BACKGROUND
  Conjugated linoleic acid (CLA) describes positional isomers of linoleic acid (LA). Experimental health benefits of CLA include amelioration of malignancy and inflammatory disease and reduction of adiposity. The Han:SPRD-cy rat model of polycystic kidney disease (PKD) features prominent renal interstitial inflammation and fibrosis that is amenable to dietary modification. We studied CLA supplementation in the modification of inflammatory outcomes in the Han:SPRD-cy rat.
  
  
  METHODS
  Male offspring of Han:SPRD-cy heterozygotes were fed diets, using corn oil or corn oil with a CLA enriched oil (1% of diet by weight as CLA). After 8 weeks, measurements included renal function and morphometry, ex vivo release of renal prostaglandin E2 (PGE2), and renal and hepatic tissue fatty acid profiles.
  
  
  RESULTS
  Urine creatinine was significantly higher in PKD animals fed CLA (P = 0.004), but differences in serum creatinine and creatinine clearance did not quite reach significance in PKD animals. CLA feeding reduced interstitial inflammation (P < 0.001), fibrosis (P = 0.03), and renal PGE2 release (P = 0.02). Cystic change and oxidized low-density lipoprotein (LDL) staining did not change significantly. CLA feeding produced increased renal and hepatic CLA isomers. Hepatic, but not renal, LA proportion was reduced on the CLA diet. The renal proportion of the PGE2 precursor, arachidonic acid (AA), was not changed by diet, but hepatic AA proportion increased significantly with CLA feeding (P= 0.009).
  
  
  CONCLUSIONS
  CLA reduces renal production of PGE2, without reduced availability of the precursor fatty acid, AA. Short-term feeding of CLA to Han:SPRD-cy rats also has significant renal anti-inflammatory and antifibrotic effects. As inflammation and fibrosis are important components of the progression of chronic renal injury, CLA may be a useful agent in dietary amelioration of renal disease.
authors.affiliation: Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba, Canada. ogborn@cc.umanitoba.ca
authors.forename: Malcolm R
authors.initials: MR
authors.lastname: Ogborn
authors.forename: Evan
authors.initials: E
authors.lastname: Nitschmann
authors.forename: Neda
authors.initials: N
authors.lastname: Bankovic-Calic
authors.forename: Hope A
authors.initials: HA
authors.lastname: Weiler
authors.forename: Shirley
authors.initials: S
authors.lastname: Fitzpatrick-Wong
authors.forename: Harold M
authors.initials: HM
authors.lastname: Aukema
mesh_terms: D000818:Animals; D016718:Arachidonic Acid / Q000378:metabolism; D003404:Creatinine / Q000652:urine; D004032:Diet; D015232:Dinoprostone / Q000037:antagonists & inhibitors*; D005355:Fibrosis; D007536:Isomerism; D007668:Kidney / Q000378:metabolism; D019787:Linoleic Acid / Q000378:metabolism; D044243:Linoleic Acids, Conjugated / Q000008:administration & dosage* / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D007690:Polycystic Kidney Diseases / Q000378:metabolism* / Q000473:pathology*; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D044243:Linoleic Acids, Conjugated; D016718:Arachidonic Acid; D019787:Linoleic Acid; D003404:Creatinine; D015232:Dinoprostone