title: Effect of gemfibrozil on the regulation of HDL subfractions in hypertriglyceridaemic patients.
abstract: OBJECTIVE
  To study changes of HDL subfractions and their regulation during gemfibrozil treatment in hypertriglyceridaemia.
  
  
  METHODS
  Twenty patients with hypertriglyceridaemia were randomized to receive either 1200 mg day-1 gemfibrozil or placebo for 3 months. After a 6-week, single-blind placebo period, the patients were randomized to receive either gemfibrozil or placebo for 3 months in a double-blind study.
  
  
  METHODS
  The patients were studied as outpatients in the Third Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland.
  
  
  METHODS
  Ultracentrifugally isolated HDL subclasses; concentrations of apoA-I, apoA-II, LpA-I and LpA-I:A-II particles; post-heparin plasma lipoprotein lipase (LPL), hepatic lipase (HL) and plasma cholesteryl ester transfer protein (CETP) activities; phospholipid transfer protein (PLTP) and lecithine cholesteryl acyltransferase (LCAT) activities were measured in plasma from six patients from both groups.
  
  
  RESULTS
  Gemfibrozil increased the concentration of HDL cholesterol (+11.1%) because of the rise of HDL3 cholesterol (34.5%, P < 0.01). The concentration of LpA-I particles was reduced during gemfibrozil treatment (-12.4%, P < 0.05), while that of apoA-II increased (+12.3%, P < 0.01). The LpA-I to LpA-I:A-II ratio decreased significantly in the gemfibrozil group (-18.9%, P < 0.01). Gemfibrozil increased LPL and HL activities by 18.2% (P < 0.05) and by 19.6%, respectively. Plasma CETP activity was also increased during gemfibrozil treatment (+15.8%, P < 0.05).
  
  
  CONCLUSIONS
  The gemfibrozil-induced elevation of HDL3 and apoA-II may reflect the combined action of LPL, HL and CETP on plasma HDL metabolism.
authors.affiliation: Third Department of Medicine, Helsinki University, Finland.
authors.forename: J
authors.initials: J
authors.lastname: Kahri
authors.forename: T
authors.initials: T
authors.lastname: Sane
authors.forename: A
authors.initials: A
authors.lastname: van Tol
authors.forename: M R
authors.initials: MR
authors.lastname: Taskinen
mesh_terms: D000328:Adult; D016632:Apolipoprotein A-I / Q000097:blood; D016633:Apolipoprotein A-II / Q000097:blood; D001053:Apolipoproteins / Q000097:blood; D017301:Ca(2+) Mg(2+)-ATPase / Q000097:blood; D002352:Carrier Proteins / Q000097:blood; D053480:Cholesterol Ester Transfer Proteins; D002788:Cholesterol Esters / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood*; D004311:Double-Blind Method; D005260:Female; D015248:Gemfibrozil / Q000008:administration & dosage / Q000627:therapeutic use*; D006023:Glycoproteins / Q000097:blood; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood / Q000188:drug therapy*; D000960:Hypolipidemic Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008565:Membrane Proteins / Q000097:blood; D008875:Middle Aged; D049294:Phospholipid Transfer Proteins; D010743:Phospholipids / Q000097:blood; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D016632:Apolipoprotein A-I; D016633:Apolipoprotein A-II; D001053:Apolipoproteins; C506642:CETP protein, human; D002352:Carrier Proteins; D053480:Cholesterol Ester Transfer Proteins; D002788:Cholesterol Esters; D008076:Cholesterol, HDL; D006023:Glycoproteins; D000960:Hypolipidemic Agents; D008074:Lipoproteins; D008565:Membrane Proteins; D049294:Phospholipid Transfer Proteins; D010743:Phospholipids; D014280:Triglycerides; D017301:Ca(2+) Mg(2+)-ATPase; D015248:Gemfibrozil