title: Modest fructose beverage intake causes liver injury and fat accumulation in marginal copper deficient rats.
abstract: OBJECTIVE
  Dietary fructose and copper interaction may play an important role in the pathogenesis of nonalcoholic fatty liver disease. In this study, whether or not modest fructose consumption (3% fructose, w/v) (which is more closely related to the American lifestyle with regard to sugar beverage consumption) affects copper status, and causes liver injury and fat accumulation in marginal copper deficient rats was investigated.
  
  
  METHODS
  Male weanling Sprague-Dawley rats were fed either an adequate copper (6 ppm) or a marginally copper deficient (1.6 ppm) diet for 4 weeks. Deionized water or deionized water containing 3% fructose (w/v) was given ad lib.
  
  
  RESULTS
  Modest fructose consumption further impaired copper status in the marginal copper deficient rats and increased hepatic iron accumulation. Liver injury and fat accumulation were significantly induced in the marginal copper deficient rats exposed to fructose.
  
  
  CONCLUSIONS
  Our data suggest that modest fructose consumption can impair copper status and lead to hepatic iron overload, which in turn, may lead to liver injury and fatty liver in marginal copper deficient rats. This study provides important information on dietary fructose and copper interaction, suggesting that dietary fructose-induced low copper availability might be an important mechanism underlying fructose-induced fatty liver.
authors.affiliation: Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Louisville School of Medicine, Louisville, Kentucky, USA.
authors.forename: Ming
authors.initials: M
authors.lastname: Song
authors.forename: Dale A
authors.initials: DA
authors.lastname: Schuschke
authors.forename: Zhanxiang
authors.initials: Z
authors.lastname: Zhou
authors.forename: Theresa
authors.initials: T
authors.lastname: Chen
authors.forename: Xue
authors.initials: X
authors.lastname: Shi
authors.forename: Jiayuan
authors.initials: J
authors.lastname: Zhang
authors.forename: Xiang
authors.initials: X
authors.lastname: Zhang
authors.forename: William M
authors.initials: WM
authors.lastname: Pierce
authors.forename: W Thomas
authors.initials: WT
authors.lastname: Johnson
authors.forename: Miriam B
authors.initials: MB
authors.lastname: Vos
authors.forename: Craig J
authors.initials: CJ
authors.lastname: McClain
mesh_terms: D000818:Animals; D001628:Beverages; D001682:Biological Availability; D018932:Chemokine CCL2 / Q000378:metabolism; D003300:Copper / Q000008:administration & dosage / Q000097:blood / Q000172:deficiency* / Q000493:pharmacokinetics; D005234:Fatty Liver / Q000139:chemically induced / Q000473:pathology*; D005632:Fructose / Q000008:administration & dosage / Q000009:adverse effects*; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D007150:Immunohistochemistry; D019190:Iron Overload / Q000139:chemically induced / Q000473:pathology; D008099:Liver / Q000473:pathology*; D008297:Male; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D000072105:Superoxide Dismutase-1; D014280:Triglycerides / Q000378:metabolism
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D014280:Triglycerides; D005632:Fructose; D003300:Copper; C000606292:Sod1 protein, rat; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D005978:Glutathione; D019803:Glutathione Disulfide