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Long-term effect of bezafibrate on pancreatic beta-cell function and insulin resistance in patients with diabetes??Original Research ArticleAtherosclerosis, Volume 194, Issue 1, September 2007, Pages 265-271Helena Tenenbaum, Solomon Behar, Valentina Boyko, Yehuda Adler, Enrique Z. Fisman, David Tanne, Mordechai Lapidot, Ehud Schwammenthal, Micha Feinberg, Zipora Matas, Michael Motro, Alexander Tenenbaum ?Close preview??|?? Related articles??|??Related reference work articles???? AbstractAbstract | Figures/TablesFigures/Tables | ReferencesReferences Abstract Objective Development of insulin resistance (IR) and the progressive failure of the pancreatic beta-cell function (BCF) may be important in the pathogenesis of type 2 diabetes. Influence of peroxisome proliferator-activated receptors ligand bezafibrate on BCF and IR in patients with diabetes is unknown. The present study was aimed to investigate the long-term effect of bezafibrate on these parameters in diabetic patients enrolled in the Bezafibrate Infarction Prevention (BIP) Study. Methods Metabolic and inflammatory parameters were analyzed from stored frozen plasma samples obtained from 351 diabetic patients (168 treated by bezafibrate and 183 by placebo) who completed a 2-year of randomized, double-blind, placebo-controlled study period. The homeostatic indexes of BCF (HOMA-BCF) and IR (HOMA-IR) were calculated according to the homeostasis model of assessment. Results Both groups displayed similar baseline characteristics. During follow-up, in the placebo group there was 28% rise of HOMA-IR (p??0.001). In contrast, HOMA-IR in patients in the bezafibrate group did not change (p?=?0.99). The intergroup differences in HOMA-IR percentage changes were in favor of bezafibrate (p?=?0.01). HOMA-BCF values have significantly decreased by 13.9% (p?=?0.04) in patients of placebo group, whereas in patients of bezafibrate group HOMA-BCF was stable during follow-up and its alterations (?2.9%) were non-significant (p?=