title: Fructose-enriched diet modifies antioxidant status and lipid metabolism in spontaneously hypertensive rats.
abstract: OBJECTIVE
  High-fructose consumption in industrial countries has been shown to induce metabolic abnormalities or syndrome X. Changes in antioxidant defense are unknown in hypertension associated with metabolic disorders induced by high-fructose feeding.
  
  
  METHODS
  Twenty spontaneously hypertensive rats were assigned to one of two groups; one received a fructose-enriched diet (60% fructose) and the other a starch diet. After a 13-wk diet period, total antioxidant status was assessed in the blood and liver by monitoring the rate of free radical-induced red blood cell hemolysis. Antioxidants (enzymes and vitamins) were determined in blood and liver. Gene expression of antioxidant enzymes (copper/zinc superoxide dismutase and glutathione peroxidase) were also investigated in hepatic tissue.
  
  
  RESULTS
  Fructose-fed rats showed blood pressure values similar to that of control rats but had increased glycemia and insulinemia. The antioxidant capacity in the blood of the fructose-fed group represented by copper/zinc superoxide dismutase and glutathione peroxidase activities and ascorbic acid was lower. However, the fructose diet enhanced the total antioxidant capacity of liver correlated with increased antioxidant enzyme activities and retinol concentrations. Gutathione peroxidase mRNA expression was decreased in livers of spontaneously hypertensive rats fed the fructose diet.
  
  
  CONCLUSIONS
  Fructose feeding negatively affects antioxidant capacity in the blood of hypertensive rats but improves this capacity in the liver.
authors.affiliation: UPRES Lipides Nutrition EA 2422, Faculté des Sciences Gabriel, Université de Bourgogne, Dijon, France. aurelie.girard@u-bourgogne.fr
authors.forename: Aurélie
authors.initials: A
authors.lastname: Girard
authors.forename: Sihem
authors.initials: S
authors.lastname: Madani
authors.forename: Farida
authors.initials: F
authors.lastname: Boukortt
authors.forename: Mustapha
authors.initials: M
authors.lastname: Cherkaoui-Malki
authors.forename: Jacques
authors.initials: J
authors.lastname: Belleville
authors.forename: Josiane
authors.initials: J
authors.lastname: Prost
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000032:analysis*; D001205:Ascorbic Acid / Q000032:analysis / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D004032:Diet; D004912:Erythrocytes / Q000737:chemistry; D005632:Fructose / Q000008:administration & dosage*; D015870:Gene Expression; D005979:Glutathione Peroxidase / Q000032:analysis / Q000097:blood / Q000235:genetics; D006973:Hypertension / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D050356:Lipid Metabolism / Q000187:drug effects*; D015227:Lipid Peroxidation; D008099:Liver / Q000737:chemistry / Q000201:enzymology; D008297:Male; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D011918:Rats, Inbred SHR; D013213:Starch / Q000008:administration & dosage; D013482:Superoxide Dismutase / Q000032:analysis / Q000097:blood / Q000235:genetics; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014801:Vitamin A / Q000032:analysis / Q000097:blood; D024502:alpha-Tocopherol / Q000032:analysis / Q000097:blood
chemical_list: D000975:Antioxidants; D001786:Blood Glucose; D007328:Insulin; D012333:RNA, Messenger; D017392:Thiobarbituric Acid Reactive Substances; D014801:Vitamin A; D005632:Fructose; D013213:Starch; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D024502:alpha-Tocopherol; D001205:Ascorbic Acid