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Phospholipid transfer protein deficiency ameliorates diet-induced hypercholesterolemia and inflammation in mice.

Abstract
Phospholipid transfer protein (PLTP) facilitates the transfer of phospholipids from triglyceride-rich lipoproteins into HDL. PLTP has been shown to be an important factor in lipoprotein metabolism and atherogenesis. Here, we report that chronic high-fat, high-cholesterol diet feeding markedly increased plasma cholesterol levels in C57BL/6 mice. PLTP deficiency attenuated diet-induced hypercholesterolemia by dramatically reducing apolipoprotein E-rich lipoproteins (-88%) and, to a lesser extent, LDL (-40%) and HDL (-35%). Increased biliary cholesterol secretion, indicated by increased hepatic ABCG5/ABCG8 gene expression, and decreased intestinal cholesterol absorption may contribute to the lower plasma cholesterol in PLTP-deficient mice. The expression of proinflammatory genes (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) is reduced in aorta of PLTP knockout mice compared with wild-type mice fed either a chow or a high-cholesterol diet. Furthermore, plasma interleukin-6 levels are significantly lower in PLTP-deficient mice, indicating reduced systemic inflammation. These data suggest that PLTP appears to play a proatherogenic role in diet-induced hyperlipidemic mice.
AuthorsLorraine Shelly, Lori Royer, Thomas Sand, Heather Jensen, Yi Luo
JournalJournal of lipid research (J Lipid Res) Vol. 49 Issue 4 Pg. 773-81 (Apr 2008) ISSN: 0022-2275 [Print] United States
PMID18198166 (Publication Type: Journal Article)
Chemical References
  • Interleukin-6
  • Lipids
  • Phospholipid Transfer Proteins
  • Intercellular Adhesion Molecule-1
Topics
  • Animal Feed
  • Animals
  • Aorta (drug effects, metabolism)
  • Gene Expression Regulation (drug effects)
  • Genotype
  • Hypercholesterolemia (genetics, metabolism)
  • Inflammation (genetics, metabolism)
  • Intercellular Adhesion Molecule-1 (genetics)
  • Interleukin-6 (blood)
  • Lipids (blood, pharmacology)
  • Liver (drug effects, metabolism)
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Phospholipid Transfer Proteins (deficiency, genetics, metabolism)

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