title: Long-term effect of bezafibrate on pancreatic beta-cell function and insulin resistance in patients with diabetes.
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=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.
authors.affiliation: Endocrinology and Diabetes Unit, Dan-Petah-Tikva District, Clalit Health Services, Israel.
authors.forename: Helena
authors.initials: H
authors.lastname: Tenenbaum
authors.forename: Solomon
authors.initials: S
authors.lastname: Behar
authors.forename: Valentina
authors.initials: V
authors.lastname: Boyko
authors.forename: Yehuda
authors.initials: Y
authors.lastname: Adler
authors.forename: Enrique Z
authors.initials: EZ
authors.lastname: Fisman
authors.forename: David
authors.initials: D
authors.lastname: Tanne
authors.forename: Mordechai
authors.initials: M
authors.lastname: Lapidot
authors.forename: Ehud
authors.initials: E
authors.lastname: Schwammenthal
authors.forename: Micha
authors.initials: M
authors.lastname: Feinberg
authors.forename: Zipora
authors.initials: Z
authors.lastname: Matas
authors.forename: Michael
authors.initials: M
authors.lastname: Motro
authors.forename: Alexander
authors.initials: A
authors.lastname: Tenenbaum
mesh_terms: D000368:Aged; D001629:Bezafibrate / Q000008:administration & dosage*; D001786:Blood Glucose; D003924:Diabetes Mellitus, Type 2 / Q000188:drug therapy* / Q000378:metabolism; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006706:Homeostasis / Q000187:drug effects; D006801:Humans; D000960:Hypolipidemic Agents / Q000008:administration & dosage*; D007249:Inflammation / Q000378:metabolism; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000502:physiology; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D010919:Placebos
chemical_list: D001786:Blood Glucose; D000960:Hypolipidemic Agents; D008055:Lipids; D010919:Placebos; D001629:Bezafibrate