title: Reciprocal metabolic perturbations in the adipose tissue and liver of GPIHBP1-deficient mice.
abstract: OBJECTIVE
  Gpihbp1-deficient (Gpihbp1-/-) mice lack the ability to transport lipoprotein lipase to the capillary lumen, resulting in mislocalization of lipoprotein lipase within tissues, defective lipolysis of triglyceride-rich lipoproteins, and chylomicronemia. We asked whether GPIHBP1 deficiency and mislocalization of catalytically active lipoprotein lipase would alter the composition of triglycerides in adipose tissue or perturb the expression of lipid biosynthetic genes. We also asked whether perturbations in adipose tissue composition and gene expression, if they occur, would be accompanied by reciprocal metabolic changes in the liver.
  
  
  RESULTS
  The chylomicronemia in Gpihbp1-/- mice was associated with reduced levels of essential fatty acids in adipose tissue triglycerides and increased expression of lipid biosynthetic genes. The liver exhibited the opposite changes: increased levels of essential fatty acids in triglycerides and reduced expression of lipid biosynthetic genes.
  
  
  CONCLUSIONS
  Defective lipolysis in Gpihbp1-/- mice causes reciprocal metabolic perturbations in adipose tissue and liver. In adipose tissue, the essential fatty acid content of triglycerides is reduced and lipid biosynthetic gene expression is increased, whereas the opposite changes occur in the liver.
authors.affiliation: 695 Charles E. Young Dr S, Los Angeles, CA 90095, USA.
authors.forename: Michael M
authors.initials: MM
authors.lastname: Weinstein
authors.forename: Christopher N
authors.initials: CN
authors.lastname: Goulbourne
authors.forename: Brandon S J
authors.initials: BS
authors.lastname: Davies
authors.forename: Yiping
authors.initials: Y
authors.lastname: Tu
authors.forename: Richard H
authors.initials: RH
authors.lastname: Barnes
authors.forename: Steven M
authors.initials: SM
authors.lastname: Watkins
authors.forename: Ryan
authors.initials: R
authors.lastname: Davis
authors.forename: Karen
authors.initials: K
authors.lastname: Reue
authors.forename: Peter
authors.initials: P
authors.lastname: Tontonoz
authors.forename: Anne P
authors.initials: AP
authors.lastname: Beigneux
authors.forename: Loren G
authors.initials: LG
authors.lastname: Fong
authors.forename: Stephen G
authors.initials: SG
authors.lastname: Young
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D005227:Fatty Acids / Q000378:metabolism; D050356:Lipid Metabolism / Q000502:physiology*; D008066:Lipolysis / Q000502:physiology; D008071:Lipoprotein Lipase / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D023421:Models, Animal; D018110:Receptors, Lipoprotein / Q000172:deficiency* / Q000235:genetics; D014280:Triglycerides / Q000378:metabolism
chemical_list: D005227:Fatty Acids; C472779:GPI-HBP1 protein, mouse; D018110:Receptors, Lipoprotein; D014280:Triglycerides; D008071:Lipoprotein Lipase