title: Feeding soy protein isolate and n-3 PUFA affects polycystic liver disease progression in a PCK rat model of autosomal polycystic kidney disease.
abstract: OBJECTIVE
  In polycystic liver disease (PCLD), multiple cysts cause liver enlargement, structural damage, and loss of function. Soy protein and dietary ω-3 polyunsaturated fatty acids (n-3 PUFAs) have been found to decrease cyst proliferation and inflammation in polycystic kidney disease. Therefore, the aim of the study was to investigate whether soy protein and n-3 PUFA supplementation attenuates PCLD.
  
  
  METHODS
  Young (age 28 days) female PCK rats were fed (n = 12 per group) either casein + corn oil (casein + CO), casein + soybean oil (casein + SO), soy protein isolate + soybean oil (SPI + SO), or SPI + 1:1 soybean/salmon oil blend (SPI + SB) diet for 12 weeks. Liver histology, gene expression by real-time quantitative polymerase chain reaction, and serum markers of liver injury were determined.
  
  
  RESULTS
  Diet had no effect on PCLD progression as indicated by no significant differences in liver weight and hepatic proliferation gene expression between diet groups. PCK rats fed SPI + SB diet, however, had the greatest (P < 0.05) histological evidence of hepatic cyst obstruction, portal inflammation, steatosis, and upregulation (P = 0.03) of fibrosis-related genes. Rats fed SPI + SB diet also had the lowest (P < 0.001) serum cholesterol and higher (P < 0.05) serum alkaline phosphatase and bilirubin concentrations.
  
  
  CONCLUSIONS
  Feeding young female PCK rats SPI and n-3 PUFA failed to attenuate PCLD progression. Furthermore, feeding SPI + SB diet resulted in complications of hepatic steatosis attributable to cysts obstruction of bile duct and hepatic vein. Based on the results, it was concluded that diet intervention alone was not effective at attenuating PCLD associated with autosomal recessive polycystic kidney disease.
authors.affiliation: *Division of Animal and Nutritional Sciences †Division of Plant and Soil Sciences ‡Department of Chemistry, West Virginia University, Morgantown §United Hospital, Bridgeport, WV.
authors.forename: Kaitlin H
authors.initials: KH
authors.lastname: Maditz
authors.forename: Vagner A
authors.initials: VA
authors.lastname: Benedito
authors.forename: Chris
authors.initials: C
authors.lastname: Oldaker
authors.forename: Nainika
authors.initials: N
authors.lastname: Nanda
authors.forename: Sundus S
authors.initials: SS
authors.lastname: Lateef
authors.forename: Ryan
authors.initials: R
authors.lastname: Livengood
authors.forename: Janet C
authors.initials: JC
authors.lastname: Tou
mesh_terms: D000469:Alkaline Phosphatase / Q000097:blood; D000818:Animals; D001652:Bile Ducts / Q000187:drug effects / Q000473:pathology; D001663:Bilirubin / Q000097:blood; D002784:Cholesterol / Q000097:blood; D003560:Cysts / Q000188:drug therapy / Q000209:etiology; D004032:Diet; D019587:Dietary Supplements; D018450:Disease Progression; D015525:Fatty Acids, Omega-3 / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use; D005234:Fatty Liver / Q000097:blood / Q000209:etiology; D005260:Female; D006503:Hepatic Veins / Q000187:drug effects / Q000473:pathology; D007249:Inflammation / Q000188:drug therapy / Q000209:etiology; D008099:Liver / Q000187:drug effects*; D008103:Liver Cirrhosis / Q000097:blood / Q000209:etiology / Q000235:genetics; D008107:Liver Diseases / Q000188:drug therapy / Q000209:etiology; D017044:Polycystic Kidney, Autosomal Recessive / Q000188:drug therapy / Q000473:pathology*; D051381:Rats; D030262:Soybean Proteins / Q000009:adverse effects / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D015525:Fatty Acids, Omega-3; D030262:Soybean Proteins; D002784:Cholesterol; D000469:Alkaline Phosphatase; D001663:Bilirubin