title: ApoE and the role of very low density lipoproteins in adipose tissue inflammation.
abstract: OBJECTIVE
  To identify the role of triglyceride-rich lipoproteins (TGRLs) and apoE, a major apolipoprotein in TGRLs, in adipose tissue inflammation with high-fat diet (HFD)-induced obesity.
  
  
  METHODS
  Male apoE(-/-) and C57BL/6J wild-type (WT) mice fed HFD for 12 weeks were assessed for metabolic and inflammatory parameters. ApoE(-/-) and WT mice were orally gavaged with [(3)H]palmitic acid to examine the role of apoE in fat delivery to adipose tissue. VLDL from obese apoE(-/-) mice were intravenously injected into lean WT or apoE(-/-) mice to test potential contribution of TGRLs-derived fat delivery to inflammation in adipose tissue and the role of apoE.
  
  
  RESULTS
  ApoE(-/-) mice gained less body weight, and had less fat mass and lower triglyceride levels in skeletal muscle than WT. ApoE(-/-) mice on HFD had better insulin sensitivity than WT even when comparing body weight-matched mice. Compared to WT mice, apoE(-/-) mice on HFD had lower levels of inflammatory cytokines/chemokines and CD11c in adipose tissue, and lower levels of inflammatory markers in skeletal muscle. At 6 h after oral gavage with [(3)H]palmitic acid, incorporation of [(3)H]palmitic acid into adipose tissue and skeletal muscle was lower in apoE(-/-) mice. After repeated daily injection for 3 days, VLDL from obese apoE(-/-) mice induced inflammation in adipose tissue of recipient WT but not apoE(-/-) mice.
  
  
  CONCLUSIONS
  In HFD-induced obesity, apoE plays an important role in inflammation in adipose tissue and skeletal muscle, likely by mediating TGRL-derived fat delivery to these tissues.
authors: Division of Atherosclerosis and Vascular Medicine, Section of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, 6565 Fannin, M.S. A-601, Houston, TX 77030, USA.
authors: Jiali
authors: J
authors: Wang
authors: Xiaoyuan Dai
authors: XD
authors: Perrard
authors: Jerry L
authors: JL
authors: Perrard
authors: Aparna
authors: A
authors: Mukherjee
authors: Corina
authors: C
authors: Rosales
authors: Yuguo
authors: Y
authors: Chen
authors: C Wayne
authors: CW
authors: Smith
authors: Henry J
authors: HJ
authors: Pownall
authors: Christie M
authors: CM
authors: Ballantyne
authors: Huaizhu
authors: H
authors: Wu
mesh_terms: D000273:Adipose Tissue / Q000276:immunology / Q000378:metabolism*; D050154:Adiposity; D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D001786:Blood Glucose / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D059305:Diet, High-Fat; D004195:Disease Models, Animal; D018836:Inflammation Mediators / Q000378:metabolism; D007275:Injections, Intravenous; D007328:Insulin / Q000097:blood; D008079:Lipoproteins, VLDL / Q000008:administration & dosage / Q000378:metabolism*; D008099:Liver / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018482:Muscle, Skeletal / Q000378:metabolism; D009765:Obesity / Q000209:etiology / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D018384:Oxidative Stress; D019308:Palmitic Acid / Q000008:administration & dosage / Q000378:metabolism; D015434:Panniculitis / Q000209:etiology / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000517:prevention & control; D013997:Time Factors; D014280:Triglycerides / Q000008:administration & dosage / Q000378:metabolism*; D015430:Weight Gain
chemical_list: D001057:Apolipoproteins E; D001786:Blood Glucose; D016207:Cytokines; D018836:Inflammation Mediators; D007328:Insulin; D008079:Lipoproteins, VLDL; D014280:Triglycerides; C030106:very low density lipoprotein triglyceride; D019308:Palmitic Acid