title: Gemfibrozil treatment potentiates oxidative resistance of high-density lipoprotein in hypertriglyceridemic patients.
abstract: BACKGROUND
  Studies suggest that both oxidized low and high density lipoprotein (LDL and HDL) play a role in the pathogenesis of atherosclerosis. Gemfibrozil is widely used and is reported to increase cholesterol of LDL and HDL in hypertriglyceridemic patients. The aim of this study was to investigate the effect of gemfibrozil treatment on the oxidative status of lipoprotein particles in Fredrickson phenotype IV hypertriglyceridemic patients.
  
  
  METHODS
  Twenty-two patients, aged 38-64 years, with fasting plasma triglyceride concentrations between 2.90 and 8.97 mmol L(-1), were recruited and were given gemfibrozil 300 mg three times daily for 12 weeks. Venous blood samples were collected before gemfibrozil treatment, after 4, 8, or 12 weeks of treatment, and 4 weeks after termination of treatment, and used to analyse the plasma lipid profile, isolate lipoproteins, and analyse the chemical composition and in vitro oxidation of lipoprotein particles.
  
  
  RESULTS
  Gemfibrozil treatment resulted in a decrease in plasma total triglyceride levels and the triglyceride content of all lipoproteins. Plasma total cholesterol levels were decreased as a result of a decrease in very low density lipoprotein (VLDL) cholesterol levels. A slight increase in LDL cholesterol levels was observed, whereas the thiobarbituric acid-reactive substances (TBARS) of LDL were decreased and the lag and peak time of LDL to oxidation were unchanged and maximal diene production was decreased. Plasma HDL cholesterol levels, the surface-to-core ratio of HDL particles, and the resistance of HDL to oxidation were increased.
  
  
  CONCLUSIONS
  The decreased TBARS and diene production of LDL, increased HDL cholesterol levels, and increased resistance of HDL to oxidation may, in part, explain why gemfibrozil treatment was found to be generally beneficial in terms of protection against coronary heart disease.
authors.affiliation: Department of Internal Medicine (Cardiology), National Taiwan University Medical Center, Taipei, Taiwan.
authors.forename: M F
authors.initials: MF
authors.lastname: Chen
authors.forename: T D
authors.initials: TD
authors.lastname: Wang
authors.forename: H T
authors.initials: HT
authors.lastname: Yeh
authors.forename: H C
authors.initials: HC
authors.lastname: Hsu
authors.forename: Y T
authors.initials: YT
authors.lastname: Lee
mesh_terms: D000284:Administration, Oral; D000328:Adult; D008076:Cholesterol, HDL / Q000378:metabolism*; D008078:Cholesterol, LDL / Q000378:metabolism; D005260:Female; D015248:Gemfibrozil / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D015228:Hypertriglyceridemia / Q000188:drug therapy* / Q000378:metabolism*; D000960:Hypolipidemic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D015227:Lipid Peroxidation; D008079:Lipoproteins, VLDL / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010084:Oxidation-Reduction; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D013997:Time Factors; D014810:Vitamin E / Q000378:metabolism
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D000960:Hypolipidemic Agents; D008079:Lipoproteins, VLDL; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D015248:Gemfibrozil