title: Rosuvastatin treatment is associated with an increase in insulin resistance in hyperlipidaemic patients with impaired fasting glucose.
abstract: OBJECTIVE
  The increase in physician-reported diabetes following rosuvastatin treatment in the Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin study has raised concerns whether this statin exerts a detrimental effect on glucose metabolism. We assessed the effect of rosuvastatin treatment across dose range on glucose homeostasis in hyperlipidaemic patients with impaired fasting glucose (IFG), who are at high risk to develop diabetes mellitus.
  
  
  METHODS
  The medical records of 72 hypelipidaemic patients with IFG on rosuvastatin 10 (RSV10 group), 20 (RSV20 group) and 40 mg/day (RSV40 group) were reviewed. The median follow up was 12.4 weeks. At the first visit, prior to rosuvastatin prescription and at the latest visit, serum lipid profile and indices of glucose metabolism, including fasting glucose, insulin and HOmeostasis Model Assessment (HOMA(IR)) index levels, were assessed.
  
  
  RESULTS
  Rosuvastatin treatment improved lipid profile and was associated with a dose-dependent significant increase in HOMA(IR) values by 25.4%, 32.3% and 44.8% at the dose of 10, 20 and 40 mg/day (p < 0.01 for all, p < 0.05 for the comparison between groups), respectively, mirrored by correspondent increase in plasma insulin levels [by 21.7%, 25.7% and 46.2% in the RSV10, RSV20 and RSV40 group (p < 0.001 for all) respectively]. Baseline HOMA(IR) levels was the most important contributor (R(2) = 68.1%, p < 0.001), followed by the dose of rosuvastatin treatment (R(2) = 23.7%, p < 0.01), in a model that explained 91.8% of the variability in HOMA(IR) increase.
  
  
  CONCLUSIONS
  In patients with IFG and hyperlipidaemia, rosuvastatin treatment was associated with a dose-dependent increase in insulin resistance.
authors.affiliation: Department of Internal Medicine, School of Medicine, University of Ioannina, Ioannina, Greece.
authors.forename: M S
authors.initials: MS
authors.lastname: Kostapanos
authors.forename: H J
authors.initials: HJ
authors.lastname: Milionis
authors.forename: A-D
authors.initials: AD
authors.lastname: Agouridis
authors.forename: C V
authors.initials: CV
authors.lastname: Rizos
authors.forename: M S
authors.initials: MS
authors.lastname: Elisaf
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000187:drug effects*; D005215:Fasting / Q000097:blood; D005260:Female; D005464:Fluorobenzenes / Q000009:adverse effects*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000009:adverse effects*; D006949:Hyperlipidemias / Q000188:drug therapy*; D000960:Hypolipidemic Agents / Q000009:adverse effects*; D007333:Insulin Resistance / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D011743:Pyrimidines / Q000009:adverse effects*; D000068718:Rosuvastatin Calcium; D013449:Sulfonamides / Q000009:adverse effects*; D055815:Young Adult
chemical_list: D001786:Blood Glucose; D005464:Fluorobenzenes; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D011743:Pyrimidines; D013449:Sulfonamides; D000068718:Rosuvastatin Calcium