title: Essential fatty acids deficiency promotes lipogenic gene expression and hepatic steatosis through the liver X receptor.
abstract: OBJECTIVE
  Nutrients influence non-alcoholic fatty liver disease. Essential fatty acids deficiency promotes various syndromes, including hepatic steatosis, through increased de novo lipogenesis. The mechanisms underlying such increased lipogenic response remain unidentified.
  
  
  METHODS
  We used wild type mice and mice lacking Liver X Receptors to perform a nutrigenomic study that aimed at examining the role of these transcription factors.
  
  
  RESULTS
  We showed that, in the absence of Liver X Receptors, essential fatty acids deficiency does not promote steatosis. Consistent with this, Liver X Receptors are required for the elevated expression of genes involved in lipogenesis in response to essential fatty acids deficiency.
  
  
  CONCLUSIONS
  This work identifies, for the first time, the central role of Liver X Receptors in steatosis induced by essential fatty acids deficiency.
authors: INRA, TOXALIM (Research Centre in Food Toxicology), Toulouse, France.
authors: Simon
authors: S
authors: Ducheix
authors: Alexandra
authors: A
authors: Montagner
authors: Arnaud
authors: A
authors: Polizzi
authors: Frédéric
authors: F
authors: Lasserre
authors: Alice
authors: A
authors: Marmugi
authors: Justine
authors: J
authors: Bertrand-Michel
authors: Normand
authors: N
authors: Podechard
authors: Talal
authors: T
authors: Al Saati
authors: Maud
authors: M
authors: Chétiveaux
authors: Silvère
authors: S
authors: Baron
authors: Jérôme
authors: J
authors: Boué
authors: Gilles
authors: G
authors: Dietrich
authors: Laila
authors: L
authors: Mselli-Lakhal
authors: Philippe
authors: P
authors: Costet
authors: Jean-Marc A
authors: JM
authors: Lobaccaro
authors: Thierry
authors: T
authors: Pineau
authors: Vassilia
authors: V
authors: Theodorou
authors: Catherine
authors: C
authors: Postic
authors: Pascal G P
authors: PG
authors: Martin
authors: Hervé
authors: H
authors: Guillou
mesh_terms: D000818:Animals; D002784:Cholesterol / Q000378:metabolism; D003677:Deficiency Diseases / Q000503:physiopathology; D004041:Dietary Fats / Q000494:pharmacology; D004195:Disease Models, Animal; D005228:Fatty Acids, Essential / Q000172:deficiency*; D005234:Fatty Liver / Q000503:physiopathology*; D005260:Female; D015870:Gene Expression / Q000187:drug effects / Q000502:physiology*; D050155:Lipogenesis / Q000187:drug effects / Q000235:genetics* / Q000502:physiology*; D008099:Liver / Q000378:metabolism; D000071518:Liver X Receptors; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008822:Mice, Transgenic; D057093:Orphan Nuclear Receptors / Q000172:deficiency / Q000235:genetics / Q000502:physiology*; D014157:Transcription Factors / Q000502:physiology; D014280:Triglycerides / Q000378:metabolism; D015854:Up-Regulation / Q000502:physiology
chemical_list: D004041:Dietary Fats; D005228:Fatty Acids, Essential; D000071518:Liver X Receptors; D057093:Orphan Nuclear Receptors; D014157:Transcription Factors; D014280:Triglycerides; D002784:Cholesterol