title: Microsomal triglyceride transfer protein in plasma and cellular lipid metabolism.
abstract: OBJECTIVE
  This review summarizes recent advances about the role of microsomal triglyceride transfer protein in plasma and tissue lipid homeostasis.
  
  
  RESULTS
  Microsomal triglyceride transfer protein emerged as a phospholipid transfer protein and acquired triacylglycerol transfer activity during evolution from invertebrates to vertebrates. These activities are proposed to participate in 'nucleation' and 'desorption' steps during the biosynthesis of primordial apoB-containing lipoproteins. Microsomal triglyceride transfer protein also transfers phospholipids to the glycolipid antigen presentation molecule CD1d. Under physiologic conditions, plasma apoB-containing lipoproteins and microsomal triglyceride transfer protein expression exhibit diurnal variations synchronized by food and light. Microsomal triglyceride transfer protein is regulated at the transcriptional level. HNF4alpha is critical for its transcription. Other transcription factors along with coactivators and corepressors modulate microsomal triglyceride transfer protein expression. Reductions in microsomal triglyceride transfer protein mRNA and activity are related to steatosis in HCV-3 infected patients. CCl4 induces steatosis by enhancing proteasomal degradation of microsomal triglyceride transfer protein and can be partially avoided by inhibiting this degradation. Chemical antagonists cause hepatosteatosis, but this was not seen in the absence of fatty acid binding protein.
  
  
  CONCLUSIONS
  Microsomal triglyceride transfer protein is a target to lower plasma lipids and to reduce inflammation in certain immune disorders. More knowledge is required, however, regarding its regulation and its role in the biosynthesis of apoB-containing lipoproteins and CD1d.
authors.affiliation: Department of Anatomy and Cell Biology, SUNY Downstate Medical Center, Brooklyn, New York 11203, USA. mhussain@downstate.edu
authors.forename: M Mahmood
authors.initials: MM
authors.lastname: Hussain
authors.forename: Paul
authors.initials: P
authors.lastname: Rava
authors.forename: Xiaoyue
authors.initials: X
authors.lastname: Pan
authors.forename: Kezhi
authors.initials: K
authors.lastname: Dai
authors.forename: Stephanie K
authors.initials: SK
authors.lastname: Dougan
authors.forename: Jahangir
authors.initials: J
authors.lastname: Iqbal
authors.forename: Farrah
authors.initials: F
authors.lastname: Lazare
authors.forename: Irani
authors.initials: I
authors.lastname: Khatun
mesh_terms: D000818:Animals; D018949:Antigens, CD1 / Q000096:biosynthesis; D055610:Antigens, CD1d; D001055:Apolipoproteins B / Q000378:metabolism; D002352:Carrier Proteins / Q000097:blood* / Q000235:genetics / Q000502:physiology; D005234:Fatty Liver / Q000378:metabolism; D005786:Gene Expression Regulation; D006801:Humans; D050356:Lipid Metabolism; D051379:Mice; D014158:Transcription, Genetic
chemical_list: D018949:Antigens, CD1; D055610:Antigens, CD1d; D001055:Apolipoproteins B; C526877:CD1D protein, human; D002352:Carrier Proteins; C106092:microsomal triglyceride transfer protein