title: Comparison of the effect of bezafibrate on improvement of atherogenic lipoproteins in Japanese familial combined hyperlipidemic patients with or without impaired glucose tolerance.
abstract: The effect of bezafibrate on plasma lipoproteins was investigated in Japanese familial combined hyperlipidemic patients with or without an impaired glucose tolerance accompanied by a low-density lipoprotein subclass, with the major gradient gel peak at a particle diameter of less than 25.5 nm. Bezafibrate treatment at a dose of 400 mg/d for 12 weeks produced an antiatherogenic effect on lipoprotein profiles, as reflected by a decrease in plasma triglyceride levels, an increase in plasma high-density lipoprotein-cholesterol levels, induction of the large-size subclass of low-density lipoprotein, and disappearance of intermediate-density lipoproteins. The plasma total and low-density lipoprotein-cholesterol-lowering effect of bezafibrate was significant in patients without impaired glucose tolerance but was not significant in patients with impaired glucose tolerance. Bezafibrate increased lipoprotein lipase activity and decreased the activity of cholesteryl ester transfer protein, both in patients with or without impaired glucose tolerance. There was no difference in the distribution of signal peptide insertion/deletion or Xbal polymorphisms of the apolipoprotein B gene in patients with or without impaired glucose tolerance. Mechanisms other than lipoprotein lipase, cholesteryl ester transfer protein activities, and an apolipoprotein B gene polymorphism may be responsible for the resistance to lowering of plasma total and low-density lipoprotein cholesterol levels with bezafibrate treatment in familial combined hyperlipidemic patients with impaired glucose tolerance.
authors.affiliation: First Department of Internal Medicine, Hiroshima University School of Medicine, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Hayashi
authors.forename: H
authors.initials: H
authors.lastname: Kurushima
authors.forename: Y
authors.initials: Y
authors.lastname: Kuga
authors.forename: T
authors.initials: T
authors.lastname: Shingu
authors.forename: K
authors.initials: K
authors.lastname: Tanaka
authors.forename: Y
authors.initials: Y
authors.lastname: Yasunobu
authors.forename: K
authors.initials: K
authors.lastname: Nomura
authors.forename: H
authors.initials: H
authors.lastname: Ohtani
authors.forename: T
authors.initials: T
authors.lastname: Hiraga
authors.forename: Y
authors.initials: Y
authors.lastname: Toyota
authors.forename: T
authors.initials: T
authors.lastname: Katano
authors.forename: K
authors.initials: K
authors.lastname: Sakai-Ohta
authors.forename: G
authors.initials: G
authors.lastname: Kajiyama
mesh_terms: D000328:Adult; D000368:Aged; D001055:Apolipoproteins B / Q000235:genetics; D001629:Bezafibrate / Q000627:therapeutic use*; D002352:Carrier Proteins / Q000097:blood; D053480:Cholesterol Ester Transfer Proteins; D002788:Cholesterol Esters / Q000097:blood; D005260:Female; D005951:Glucose Tolerance Test; D006023:Glycoproteins; D006801:Humans; D006950:Hyperlipidemia, Familial Combined / Q000097:blood / Q000188:drug therapy* / Q000235:genetics; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008071:Lipoprotein Lipase / Q000097:blood; D008074:Lipoproteins / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008875:Middle Aged
chemical_list: D001055:Apolipoproteins B; C506642:CETP protein, human; D002352:Carrier Proteins; D053480:Cholesterol Ester Transfer Proteins; D002788:Cholesterol Esters; D006023:Glycoproteins; D000960:Hypolipidemic Agents; D008074:Lipoproteins; D008077:Lipoproteins, LDL; D008071:Lipoprotein Lipase; D001629:Bezafibrate