title: Attenuation of progression of insulin resistance in patients with coronary artery disease by bezafibrate.
abstract: BACKGROUND
  Development of insulin resistance (IR) may be important in the pathogenesis of both metabolic syndrome and type 2 diabetes mellitus. Few data are available regarding the short-term efficacy of the peroxisome proliferator-activated receptor ligand bezafibrate on IR, and its long-term effect is unknown. The present analysis aimed to investigate the effect of bezafibrate on IR in patients with coronary artery disease enrolled in the Bezafibrate Infarction Prevention Study.
  
  
  METHODS
  Metabolic and inflammatory parameters were analyzed from stored frozen plasma samples obtained from patients who completed a 2-year, randomized, double-blind, placebo-controlled study. The homeostatic indexes of IR (HOMA-IRs) were calculated according to the homeostasis model of assessment.
  
  
  RESULTS
  Both the patients taking bezafibrate (n = 1262) and those taking placebo (n = 1242) displayed similar baseline characteristics. The HOMA-IRs significantly correlated at baseline and during follow-up with glucose (r = 0.35 and 0.31, respectively) and triglycerides (r = 0.16 and 0.19, respectively). In a subgroup of 351 patients with diabetes, HOMA-IR at baseline was 88% higher than in their counterparts with normal glucose levels (P<.001). In the placebo group, during follow-up there was a significant 34.4% rise in HOMA-IR. In contrast, in the bezafibrate group there was only a nonsignificant 6.6% change in HOMA-IR. The intergroup differences in percentage changes of HOMA-IR were in favor of bezafibrate (P<.001).
  
  
  CONCLUSIONS
  In patients with coronary artery disease enrolled in our study, as represented by the placebo group, HOMA-IR increased over time. During the 2 years of the follow-up, bezafibrate significantly attenuated this process.
authors.affiliation: Cardiac Rehabilitation Institute, Tel-Hashomer, Israel.
authors.forename: Alexander
authors.initials: A
authors.lastname: Tenenbaum
authors.forename: Enrique Z
authors.initials: EZ
authors.lastname: Fisman
authors.forename: Valentina
authors.initials: V
authors.lastname: Boyko
authors.forename: Michal
authors.initials: M
authors.lastname: Benderly
authors.forename: David
authors.initials: D
authors.lastname: Tanne
authors.forename: Moti
authors.initials: M
authors.lastname: Haim
authors.forename: Zipora
authors.initials: Z
authors.lastname: Matas
authors.forename: Michael
authors.initials: M
authors.lastname: Motro
authors.forename: Solomon
authors.initials: S
authors.lastname: Behar
mesh_terms: D000368:Aged; D001629:Bezafibrate / Q000494:pharmacology* / Q000627:therapeutic use; D003324:Coronary Artery Disease / Q000097:blood / Q000503:physiopathology*; D003920:Diabetes Mellitus / Q000097:blood / Q000503:physiopathology; D018450:Disease Progression; D005260:Female; D006801:Humans; D000960:Hypolipidemic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D007333:Insulin Resistance; D008297:Male; D008875:Middle Aged; D047492:Peroxisome Proliferator-Activated Receptors; D016032:Randomized Controlled Trials as Topic; D014280:Triglycerides / Q000097:blood
chemical_list: D000960:Hypolipidemic Agents; D047492:Peroxisome Proliferator-Activated Receptors; D014280:Triglycerides; D001629:Bezafibrate