title: A Western-fed diet increases plasma HDL and LDL-cholesterol levels in apoD-/- mice.
abstract: OBJECTIVE
  Plasma apolipoprotein (apo)D, a ubiquitously expressed protein that binds small hydrophobic ligands, is found mainly on HDL particles. According to studies of human genetics and lipid disorders, plasma apoD levels positively correlate with HDL-cholesterol and apoAI levels. Thus, we tested the hypothesis that apoD was a regulator of HDL metabolism.
  
  
  RESULTS
  We compared the plasma lipid and lipoprotein profiles of wild-type (WT) C57BL/6 mice with apoD-/- mice on a C57BL/6 background after receiving a high fat-high cholesterol diet for 12 weeks. ApoD-/- mice had higher HDL-cholesterol levels (61±13-apoD-/- vs. 52±10-WT-males; 37±11-apoD-/- vs. 22±2 WT-female) than WT mice with sex-specific changes in total plasma levels of cholesterol and other lipids. Compared to WT, the HDL of apoD-/- mice showed an increase in large, lipid-rich HDL particles and according to size various quantities and sizes of LDL particles. Plasma levels of lecithin:cholesterol acyltransferase in the control and apoD-/- mice were not different, however, plasma phospholipid transfer protein activity was modestly elevated (+10%) only in male apoD-/- mice. An in vivo HDL metabolism experiment with isolated Western-fed apoD-/- HDL particles showed that female apoD-/- mice had a 36% decrease in the fractional catabolic rate of HDL cholesteryl ester. Hepatic SR-BI and LDLR protein levels were significantly decreased; accordingly, LDL-cholesterol and apoB levels were increased in female mice.
  
  
  CONCLUSIONS
  In the context of a high fat-high cholesterol diet, apoD deficiency in female mice is associated with increases in both plasma HDL and LDL-cholesterol levels, reflecting changes in expression of SR-BI and LDL receptors, which may impact diet-induced atherosclerosis.
authors.affiliation: The City College of New York, Biology Department, New York, New York, United States of America; Graduate Center at CUNY, New York, New York, United States of America.
authors.forename: Kamilah
authors.initials: K
authors.lastname: Ali
authors.affiliation: The City College of New York, Biology Department, New York, New York, United States of America; Graduate Center at CUNY, New York, New York, United States of America.
authors.forename: Ehab M
authors.initials: EM
authors.lastname: Abo-Ali
authors.affiliation: The City College of New York, Biology Department, New York, New York, United States of America.
authors.forename: M D
authors.initials: MD
authors.lastname: Kabir
authors.affiliation: The City College of New York, Biology Department, New York, New York, United States of America.
authors.forename: Bethany
authors.initials: B
authors.lastname: Riggins
authors.affiliation: The City College of New York, Biology Department, New York, New York, United States of America.
authors.forename: Susanna
authors.initials: S
authors.lastname: Nguy
authors.affiliation: The City College of New York, Biology Department, New York, New York, United States of America.
authors.forename: Lisa
authors.initials: L
authors.lastname: Li
authors.affiliation: The City College of New York, Biology Department, New York, New York, United States of America.
authors.forename: Ujala
authors.initials: U
authors.lastname: Srivastava
authors.affiliation: The City College of New York, Biology Department, New York, New York, United States of America.
authors.forename: Su Mya Mya
authors.initials: SM
authors.lastname: Thinn
mesh_terms: D000818:Animals; D053399:Apolipoproteins D / Q000235:genetics*; D008076:Cholesterol, HDL / Q000097:blood*; D008078:Cholesterol, LDL / Q000097:blood*; D066273:Diet, Western / Q000009:adverse effects*; D005260:Female; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D008810:Mice, Inbred C57BL; D010316:Particle Size
chemical_list: D053399:Apolipoproteins D; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL