title: Hepatic effects of a fructose diet in the stroke-prone spontaneously hypertensive rat.
abstract: BACKGROUND
  Feeding stroke-prone spontaneously hypertensive rats (SHRSP) a diet rich in fructose results in a profound glucose intolerance not observed in the normotensive Wistar Kyoto (WKY) strain. The aim of this study was to investigate the role of the liver in the underlying mechanisms in the SHRSP.
  
  
  METHODS
  SHRSP and WKY rats were fed either 60% fructose or regular chow for 2 weeks with blood pressure being measured using tail-cuff plethysmography and radiotelemetry. Intraperitoneal glucose tolerance tests were performed and livers harvested for analysis of expression of inflammatory mediators and antioxidant proteins by western blotting and quantitative reverse transcriptase-PCR. The serum triglyceride content and fatty acid profiles were also measured.
  
  
  RESULTS
  Feeding SHRSP and WKY on 60% fructose for 2 weeks resulted in glucose intolerance with no increases in levels of blood pressure. Serum triglycerides were increased in both strains of fructose-fed rats with the highest levels being observed in the SHRSP. The serum fatty acid profiles were changed with large increases in the amounts of oleic acid (18.1) and reductions in linoleic acid (18.2). Levels of expression of c-jun N-terminal kinase/stress activated protein kinase (JNK/SAPK), and nuclear factor kappaB (NF-kappaB) were shown to be unchanged between the livers of the chow and fructose-fed groups. In contrast, protein levels of the three isoforms of superoxide dismutase (SOD) were upregulated in liver of SHRSP fed on fructose while only manganese SOD (MnSOD) was upregulated in fructose-fed WKY rats.
  
  
  CONCLUSIONS
  These results demonstrate that the major contribution of the liver in the early pathogenesis of metabolic syndrome may be an increased secretion of triglyceride containing altered proportions of fatty acid pools. Feeding rats a diet rich in fructose does not affect hepatic expression of inflammatory pathways and the increased hepatic SOD expression may constitute an early protective mechanism.
authors.affiliation: Center for Metabolic Disease, Ordway Research Institute, Albany, New York, USA. jbrosnan@ordwayresearch.org
authors.forename: M Julia
authors.initials: MJ
authors.lastname: Brosnan
authors.forename: Richard D
authors.initials: RD
authors.lastname: Carkner
mesh_terms: D000818:Animals; D001794:Blood Pressure; D004040:Dietary Carbohydrates / Q000008:administration & dosage*; D005632:Fructose / Q000008:administration & dosage*; D018149:Glucose Intolerance / Q000209:etiology; D006973:Hypertension / Q000378:metabolism*; D048031:JNK Mitogen-Activated Protein Kinases / Q000032:analysis; D019787:Linoleic Acid / Q000097:blood; D008099:Liver / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome; D048055:Mitogen-Activated Protein Kinase 8 / Q000032:analysis; D016328:NF-kappa B / Q000032:analysis; D019301:Oleic Acid / Q000097:blood; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013482:Superoxide Dismutase; D014280:Triglycerides / Q000097:blood
chemical_list: D004040:Dietary Carbohydrates; D016328:NF-kappa B; D014280:Triglycerides; D019301:Oleic Acid; D005632:Fructose; D019787:Linoleic Acid; D013482:Superoxide Dismutase; D048031:JNK Mitogen-Activated Protein Kinases; D048055:Mitogen-Activated Protein Kinase 8