title: Liver fat accumulation may be dissociated from adiposity gain in ovariectomized rats.
abstract: OBJECTIVE
  The purpose of the present study was to establish a model of rats prone and resistant to intra-abdominal fat accumulation in response to ovariectomy (Ovx-P and Ovx-R) and to determine its relationship with molecular biomarkers.
  
  
  METHODS
  Two experiments were conducted in which female rats were either sham-operated (Sham) or ovariectomized (Ovx). In the first experiment, ovariectomized rats were stratified into three tertiles based on intra-abdominal adipose tissue mass. To strengthen the Ovx-P/Ovx-R model, we conducted a second experiment in which the numbers of rats in each group were extended and in which different molecular markers were measured. At the end of a 6-8-week period, ovariectomized rats that displayed the lower abdominal fat accumulation (lower tertile) were labelled as Ovx-R and those in the upper tertile as Ovx-P.
  
  
  RESULTS
  Ovx-R rats displayed similar abdominal fat gain to Sham rats whereas Ovx-P rats depicted abdominal fat mass twice as high as that of Sham and Ovx-R rats. Despite the difference in abdominal adiposity, liver fat content was ~50% higher (p < 0.01) in both Ovx-R and Ovx-P rats compared to Sham rats. In addition, both Ovx-R and Ovx-P rats depicted higher HOMA-IR scores (p < 0.05) and lower (p < 0.01) hepatic gene expression of leptin receptor-b and -e, microsomal transfer protein (MTP), and diacylglycerol acyltransferase-2 (DGAT-2) compared to Sham rats.
  
  
  CONCLUSIONS
  The present findings indicate that estrogen withdrawal-induced hepatic steatosis and associated insulin resistance may be dissociated from abdominal fat accumulation and suggest that a decrease in leptin action through a down-regulation of leptin receptors and a decrease in very low density lipoprotein production through a down-regulation of MTP and DGAT-2 may be factors responsible for this observation in the absence of peripheral fat gain.
authors.affiliation: Department of Kinesiology, Université de Montréal, Montréal, Québec, Canada.
authors.forename: I
authors.initials: I
authors.lastname: Côté
authors.forename: S
authors.initials: S
authors.lastname: Yasari
authors.forename: A
authors.initials: A
authors.lastname: Pighon
authors.forename: R
authors.initials: R
authors.lastname: Barsalani
authors.forename: R
authors.initials: R
authors.lastname: Rabasa-Lhoret
authors.forename: D
authors.initials: D
authors.lastname: Prud'homme
authors.forename: J-M
authors.initials: JM
authors.lastname: Lavoie
mesh_terms: D050153:Abdominal Fat; D050154:Adiposity / Q000502:physiology*; D000818:Animals; D002352:Carrier Proteins / Q000235:genetics; D051048:Diacylglycerol O-Acyltransferase / Q000235:genetics; D005234:Fatty Liver / Q000209:etiology* / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D007333:Insulin Resistance; D008099:Liver / Q000378:metabolism; D010052:Ovariectomy; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D054411:Receptors, Leptin / Q000235:genetics
chemical_list: D002352:Carrier Proteins; D012333:RNA, Messenger; D054411:Receptors, Leptin; C106092:microsomal triglyceride transfer protein; C494885:DGAT2 protein, human; D051048:Diacylglycerol O-Acyltransferase