Journal
ATHEROSCLEROSIS
Volume 194, Issue 1, Pages 265-271Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2006.08.005
Keywords
type 2 diabetes; bezafibrate; lipids; beta-cell function; insulin resistance; secondary prevention
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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 Bezatibrate 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 < 0.00 1). 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 = 0.59). Conclusions: Diabetic patients from the placebo group demonstrated a progressive declining of BCF and an increasing of IR over 2 years of follow-up. These longitudinal changes were attenuated when patients used bezafibrate. (c) 2006 Published by Elsevier Ireland Ltd.
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