title: Common sequence variant in lipoprotein lipase gene conferring triglyceride response to fibrate treatment.
abstract: OBJECTIVE
  Little is known about whether the variations in the lipoprotein lipase (LPL) and apolipoprotein gene cluster (APOA1/C3/A5) confer appreciable triglyceride lowering after fibrate treatment among patients with hypertriglyceridemia.
  
  
  METHODS
  We investigated whether variations in these genes confer a triglyceride lowering response after fibrate treatment among 145 patients with hypertriglyceridemia receiving 6 months of fibrate treatment.
  
  
  RESULTS
  Overall triglycerides decreased from 746.2 mg/dl to 465.9 mg/dl and the mean percentage of triglyceride lowering was 50.7 +/- 38.6%. A total of two polymorphisms, LPL IVS8 +483T>G and APOA1 +2169G>C, were associated with a significant percentage of triglyceride lowering. Common haplotype effects of LPL on the triglyceride lowering percentage were significant (p = 0.002) and the percentage of variance explained by the LPL haplotype was 7.5%. One common LPL haplotype encompassing three polymorphisms was associated with a -45.40% change (p < 0.001) and risk of a 5.9-fold risk for developing a poor response (95% confidence interval: 1.11-31, p = 0.037), compared with the most frequent LPL haplotype.
  
  
  CONCLUSIONS
  Our results indicate that the LPL gene variant may cause triglyceride lowering after fibrate treatment among patients with hypertriglyceridemia.
authors.affiliation: Institute of Preventive Medicine, School of Preventive Medicine, National Taiwan University, Taiwan.
authors.forename: Kuo-Liong
authors.initials: KL
authors.lastname: Chien
authors.forename: Yen-Lin
authors.initials: YL
authors.lastname: Lin
authors.forename: Hui-Chin
authors.initials: HC
authors.lastname: Wen
authors.forename: Hsing-Pei
authors.initials: HP
authors.lastname: Lin
authors.forename: Ching-Tzu
authors.initials: CT
authors.lastname: Yen
authors.forename: Shu-Wha
authors.initials: SW
authors.lastname: Lin
authors.forename: Jau-Tsuen
authors.initials: JT
authors.lastname: Kao
mesh_terms: D001053:Apolipoproteins / Q000235:genetics; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D002994:Clofibrate / Q000627:therapeutic use*; D005260:Female; D014644:Genetic Variation; D005838:Genotype; D006801:Humans; D015228:Hypertriglyceridemia / Q000097:blood / Q000188:drug therapy / Q000201:enzymology / Q000235:genetics*; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D007438:Introns; D008071:Lipoprotein Lipase / Q000235:genetics* / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D005810:Multigene Family; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D020641:Polymorphism, Single Nucleotide; D014280:Triglycerides / Q000378:metabolism*
chemical_list: D001053:Apolipoproteins; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D000960:Hypolipidemic Agents; D008077:Lipoproteins, LDL; D014280:Triglycerides; D002784:Cholesterol; D008071:Lipoprotein Lipase; D002994:Clofibrate