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Attenuation of Progression of Insulin Resistance in Patients With Coronary Artery Disease by Bezafibrate
Alexander Tenenbaum, MD, PhD;
Enrique Z. Fisman, MD;
Valentina Boyko, MS;
Michal Benderly, PhD;
David Tanne, MD;
Moti Haim, MD;
Zipora Matas, PhD;
Michael Motro, MD;
Solomon Behar, MD
Arch Intern Med. 2006;166:737-741.
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.
Author Affiliations: Cardiac Rehabilitation Institute (Drs Tenenbaum, Fisman, and Motro) and Bezafibrate Infarction Prevention Study Coordinating Center, Neufeld Cardiac Research Institute, Chaim Sheba Medical Center (Ms Boyko and Drs Benderly, Tanne, Haim, and Behar), Tel-Hashomer, Israel; and Biochemistry Laboratory, Wolfson Medical Center, Holon, Israel, affiliated with the Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel (Dr Matas).
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