title: Chronic dietary intake of quercetin alleviates hepatic fat accumulation associated with consumption of a Western-style diet in C57/BL6J mice.
abstract: METHODS
  To determine the effect of consumption of a quercetin-rich diet on obesity and dysregulated hepatic gene expression.
  
  
  RESULTS
  C56BL/6J mice were fed for 20 wk on AIN93G (control) or a Western diet high in fat, cholesterol and sucrose, both with or without 0.05% quercetin. Triglyceride levels in plasma, thiobarbituric acid-reactive substances (oxidative stress marker) and glutathione levels and peroxisome proliferator-activated receptor α expression in livers of mice fed with the Western diet were all improved after 8 wk feeding with quercetin. After 20 wk, further reductions of visceral and liver fat accumulation and improved hyperglycemia, hyperinsulinemia, dyslipidemia and plasma adiponectin and TNFα levels in these mice fed with quercetin were observed. The expression of hepatic genes related to steatosis, such as peroxisome proliferator-activated receptor γ and sterol regulatory element-binding protein-1c was also normalized by quercetin. In mice fed with the control diet, quercetin did not affect body weight but reduces the plasma TNFα and hepatic thiobarbituric acid-reactive substance levels.
  
  
  CONCLUSIONS
  In mice fed with a Western diet, chronic dietary intake of quercetin reduces liver fat accumulation and improves systemic parameters related to metabolic syndrome, probably mainly through decreasing oxidative stress and reducing PPARα expression, and the subsequent reduced expression in the liver of genes related to steatosis.
authors.affiliation: National Food Research Institute, National Agriculture and Food Research Organization, Tsukuba, Ibaraki, Japan. kobori@affrc.go.jp
authors.forename: Masuko
authors.initials: M
authors.lastname: Kobori
authors.forename: Saeko
authors.initials: S
authors.lastname: Masumoto
authors.forename: Yukari
authors.initials: Y
authors.lastname: Akimoto
authors.forename: Hideaki
authors.initials: H
authors.lastname: Oike
mesh_terms: D050154:Adiposity; D000818:Animals; D004032:Diet / Q000009:adverse effects; D005234:Fatty Liver / Q000209:etiology / Q000517:prevention & control*; D005786:Gene Expression Regulation; D005978:Glutathione / Q000378:metabolism; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology / Q000517:prevention & control; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D018384:Oxidative Stress; D047493:PPAR alpha / Q000235:genetics / Q000378:metabolism; D011794:Quercetin / Q000627:therapeutic use*; D012333:RNA, Messenger; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors; D014280:Triglycerides / Q000378:metabolism
chemical_list: D047493:PPAR alpha; D012333:RNA, Messenger; D051780:Sterol Regulatory Element Binding Protein 1; D017392:Thiobarbituric Acid Reactive Substances; D014280:Triglycerides; D011794:Quercetin; D005978:Glutathione