title: Bisphenol A exposure increases liver fat in juvenile fructose-fed Fischer 344 rats.
abstract: BACKGROUND
  Prenatal exposure to bisphenol A (BPA) has been shown to induce obesity in rodents. To evaluate if exposure also later in life could induce obesity or liver damage we investigated these hypothesises in an experimental rat model.
  
  
  METHODS
  From five to fifteen weeks of age, female Fischer 344 rats were exposed to BPA via drinking water (0.025, 0.25 or 2.5 mg BPA/L) containing 5% fructose. Two control groups were given either water or 5% fructose solution. Individual weight of the rats was determined once a week. At termination magnetic resonance imaging was used to assess adipose tissue amount and distribution, and liver fat content. After sacrifice the left perirenal fat pad and the liver were dissected and weighed. Apolipoprotein A-I in plasma was analyzed by western blot.
  
  
  RESULTS
  No significant effects on body weight or the weight of the dissected fad pad were seen in rats exposed to BPA, and MRI showed no differences in total or visceral adipose tissue volumes between the groups. However, MRI showed that liver fat content was significantly higher in BPA-exposed rats than in fructose controls (p=0.04). BPA exposure also increased the apolipoprotein A-I levels in plasma (p<0.0001).
  
  
  CONCLUSIONS
  We found no evidence that BPA exposure affects fat mass in juvenile fructose-fed rats. However, the finding that BPA in combination with fructose induced fat infiltration in the liver at dosages close to the current tolerable daily intake (TDI) might be of concern given the widespread use of this compound in our environment.
authors.affiliation: Occupational and Environmental Medicine, Uppsala University, Uppsala, Sweden. Electronic address: Monika.Ronn@medsci.uu.se.
authors.forename: Monika
authors.initials: M
authors.lastname: Rönn
authors.forename: Joel
authors.initials: J
authors.lastname: Kullberg
authors.forename: Helen
authors.initials: H
authors.lastname: Karlsson
authors.forename: Johan
authors.initials: J
authors.lastname: Berglund
authors.forename: Filip
authors.initials: F
authors.lastname: Malmberg
authors.forename: Jan
authors.initials: J
authors.lastname: Orberg
authors.forename: Lars
authors.initials: L
authors.lastname: Lind
authors.forename: Håkan
authors.initials: H
authors.lastname: Ahlström
authors.forename: P Monica
authors.initials: PM
authors.lastname: Lind
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D016632:Apolipoprotein A-I / Q000097:blood; D001559:Benzhydryl Compounds / Q000008:administration & dosage / Q000633:toxicity*; D015153:Blotting, Western; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology* / Q000473:pathology; D004305:Dose-Response Relationship, Drug; D005260:Female; D005632:Fructose / Q000008:administration & dosage; D050152:Intra-Abdominal Fat / Q000187:drug effects / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008279:Magnetic Resonance Imaging / Q000379:methods; D009765:Obesity / Q000139:chemically induced*; D010636:Phenols / Q000008:administration & dosage / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000473:pathology*; D051381:Rats; D011916:Rats, Inbred F344; D000098826:Bisphenol A Compounds
chemical_list: D016632:Apolipoprotein A-I; D001559:Benzhydryl Compounds; D005632:Fructose; D010636:Phenols; C006780:bisphenol A; D000098826:Bisphenol A Compounds