title: Alterations of high-density lipoprotein subclasses in hypercholesterolemia and combined hyperlipidemia.
abstract: BACKGROUND
  Alterations in plasma lipid levels can influence the composition, content, and distribution of plasma lipoprotein subclasses that effect atherosclerosis risk. Hypercholesterolemia and combined hyperlipidemia are common forms of atherogenic dyslipoproteinemia. This study evaluates the alterations of high-density lipoprotein (HDL) subclasses in hypercholesterolemic and combined hyperlipidemic subjects.
  
  
  METHODS
  Apolipoprotein A-I contents of plasma HDL subclasses were quantitated by 2-dimensional gel electrophoresis in 242 normolipidemic subjects, 66 hypercholesterolemic subjects and 59 combined hyperlipidemic subjects.
  
  
  RESULTS
  Compared with the normolipidemic subjects, apolipoprotein A-I contents of small-sized pre-beta1-HDL, HDL3c, HDL3b and HDL3a were significantly higher in both hypercholesterolemic subjects (p<.01, p<.05, p<.01 and p<.05, respectively) and combined hyperlipidemic subjects (p<.01, p<.05, p<.01 and p<.01, respectively). In contrast, apolipoprotein A-I contents of large-sized HDL2a and HDL2b were significantly lower in hypercholesterolemic subjects (p<.05 and p<.01, respectively) as well as combined hyperlipidemic subjects (p<.01 and p<.01, respectively). In addition, pre-beta1-HDL increased significantly (p<.05) while HDL2a and HDL2b decreased significantly (p<.05 and p<.01, respectively) in combined hyperlipidemic group versus hypercholesterolemic subjects. With the elevation of triglyceride levels, pre-beta1-HDL, and HDL3a increased successively, however, HDL2a and HDL2b decreased successively in subjects with total cholesterol levels greater than 240 mg/dl.
  
  
  CONCLUSIONS
  The particle size of HDL shifted towards smaller size in hypercholesterolemic subjects, and that the shift was more prominent in combined hyperlipidemic subjects. The alternations mentioned above indicate that HDL maturation might be abnormal, and reverse cholesterol transport (RCT) might be weakened.
authors.affiliation: Laboratory of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu 610041, Sichuan, PR China.
authors.forename: Lianqun
authors.initials: L
authors.lastname: Jia
authors.forename: Mingde
authors.initials: M
authors.lastname: Fu
authors.forename: Ying
authors.initials: Y
authors.lastname: Tian
authors.forename: Yanhua
authors.initials: Y
authors.lastname: Xu
authors.forename: Lantu
authors.initials: L
authors.lastname: Gou
authors.forename: Haoming
authors.initials: H
authors.lastname: Tian
authors.forename: Li
authors.initials: L
authors.lastname: Tian
mesh_terms: D000328:Adult; D000368:Aged; D001053:Apolipoproteins / Q000097:blood*; D015180:Electrophoresis, Gel, Two-Dimensional; D005260:Female; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood*; D006949:Hyperlipidemias / Q000097:blood*; D008075:Lipoproteins, HDL / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008875:Middle Aged; D014280:Triglycerides / Q000097:blood
chemical_list: D001053:Apolipoproteins; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D014280:Triglycerides