title: Comparison of free fructose and glucose to sucrose in the ability to cause fatty liver.
abstract: BACKGROUND
  There is evidence that disaccharide sucrose produce a greater increase in serum fructose and triglycerides (TGs) than the effect produced by their equivalent monosaccharides, suggesting that long-term exposure to sucrose or fructose + glucose could potentially result in different effects.
  
  
  OBJECTIVE
  We studied the chronic effects of a combination of free fructose and glucose relative to sucrose on rat liver.
  
  
  METHODS
  Rats were fed either a combination of 30% fructose and 30% glucose (FG) or 60% sucrose (S). Control rats were fed normal rat chow (C). All rats were pair fed and were followed for 4 months. After killing, blood chemistries and liver tissue were examined.
  
  
  RESULTS
  Both FG-fed- and S-fed rats developed early features of metabolic syndrome when compared with C. In addition, both diets induced hepatic alterations, including variable increases in hepatic TG accumulation and fatty liver, an increase in uric acid content in the liver, as well as an increase in hepatic levels of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) measured in liver homogenates.
  
  
  CONCLUSIONS
  Diets containing 30% of fructose either as free fructose and glucose, or as sucrose, induce metabolic syndrome, intrahepatic accumulation of uric acid and TGs, increased MCP-1 and TNF-alpha as well as fatty liver in rats. It will be relevant to determine clinically whether pharmacological reduction in uric acid levels might have a therapeutic advantage in the treatment of non-alcoholic fatty liver disease.
authors.affiliation: Division of Nephrology, Hypertension and Transplantation, University of Florida, Gainesville, FL, USA. lgsanchezlozada@gmail.com
authors.forename: Laura G
authors.initials: LG
authors.lastname: Sánchez-Lozada
authors.forename: Wei
authors.initials: W
authors.lastname: Mu
authors.forename: Carlos
authors.initials: C
authors.lastname: Roncal
authors.forename: Yuri Y
authors.initials: YY
authors.lastname: Sautin
authors.forename: Manal
authors.initials: M
authors.lastname: Abdelmalek
authors.forename: Sirirat
authors.initials: S
authors.lastname: Reungjui
authors.forename: MyPhuong
authors.initials: M
authors.lastname: Le
authors.forename: Takahiko
authors.initials: T
authors.lastname: Nakagawa
authors.forename: Hui Y
authors.initials: HY
authors.lastname: Lan
authors.forename: Xuequing
authors.initials: X
authors.lastname: Yu
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Johnson
mesh_terms: D000818:Animals; D050218:Body Fat Distribution; D018932:Chemokine CCL2 / Q000032:analysis; D004040:Dietary Carbohydrates / Q000008:administration & dosage*; D019422:Dietary Sucrose / Q000008:administration & dosage*; D002149:Energy Intake; D005234:Fatty Liver / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D005632:Fructose / Q000008:administration & dosage*; D005947:Glucose / Q000008:administration & dosage*; D008099:Liver / Q000737:chemistry; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000032:analysis / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D014527:Uric Acid / Q000032:analysis / Q000097:blood
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D004040:Dietary Carbohydrates; D019422:Dietary Sucrose; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D014527:Uric Acid; D005632:Fructose; D005947:Glucose