title: [A relationship between insulin resistance and reduction in oxidative stress in vivo by atorvastatin].
abstract: OBJECTIVE
  To examine the relationship between insulin resistance (IR) and the reduction of oxidative stress in vivo by the statin atorvastatin.
  
  
  METHODS
  This study included 40 patients with hypercholesterolemia without a history of diabetes mellitus (21 males, 19 females, mean age 62 +/- 11 years). Homeostasis assessment insulin resistance (HOMA-IR) was used as a marker for insulin resistance. The patients were divided into two groups [IR group (n = 24) and non-IR group (n = 16), using the cut off level of 1.73]. Urinary 8-iso-prostaglandin F2alpha (U-8-iso) excretion was used as an oxidative stress marker. The subjects were treated with atorvastatin (10 mg/day) for 12 weeks.
  
  
  RESULTS
  The IR group had significantly higher U-8-iso levels than the non-IR group before atorvastatin administration (211 +/- 112 vs 137 +/- 33 pg/mg Cr, p = 0.01). Low-density lipoprotein cholesterol, triglyceride, and 8-iso levels were significantly reduced in both groups after 12 weeks, U-8-iso levels were significantly higher in the IR group than the non-IR group (178 +/- 61 vs 110 +/- 38 pg/mg Cr, p = 0.003), and HOMA-IR showed no significant change. Multiple regression analysis after 12 weeks showed that HOMA-IR and triglyceride levels were independent variables for U-8-iso levels (standard regression coefficient = 0.60, 0.59, p < 0.0001, p = 0.0002).
  
  
  CONCLUSIONS
  Insulin resistance is important in the occurrence of oxidative stress in patients with hypercholesterolemia. Since atorvastatin does not reduce insulin resistance, further therapy to reduce insulin resistance is necessary for early prevention of cardiovascular events during atorvastatin treatment.
authors.affiliation: Department of Cardiovascular Center, Sakura Hospital, Toho University School of Medicine, Chiba. ddda@cc.rim.or.jp
authors.forename: Takashi
authors.initials: T
authors.lastname: Hitsumoto
authors.forename: Takuo
authors.initials: T
authors.lastname: Iizuka
authors.forename: Mao
authors.initials: M
authors.lastname: Takahashi
authors.forename: Keijirou
authors.initials: K
authors.lastname: Nakamura
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Shimizu
authors.forename: Shin
authors.initials: S
authors.lastname: Satoh
authors.forename: Yuko
authors.initials: Y
authors.lastname: Sugiyama
authors.forename: Takeshi
authors.initials: T
authors.lastname: Sakurai
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Noike
authors.forename: Hidefumi
authors.initials: H
authors.lastname: Ohsawa
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Watanabe
authors.forename: Kohji
authors.initials: K
authors.lastname: Shirai
mesh_terms: D000368:Aged; D000069059:Atorvastatin; D015237:Dinoprost / Q000031:analogs & derivatives* / Q000652:urine; D005260:Female; D006538:Heptanoic Acids / Q000494:pharmacology* / Q000627:therapeutic use; D006706:Homeostasis; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D006937:Hypercholesterolemia / Q000097:blood / Q000503:physiopathology*; D007333:Insulin Resistance; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects*; D011758:Pyrroles / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D011758:Pyrroles; C075750:8-epi-prostaglandin F2alpha; D000069059:Atorvastatin; D015237:Dinoprost