title: Vitamin E supplementation improves endothelial function in type I diabetes mellitus: a randomized, placebo-controlled study.
abstract: OBJECTIVE
  We sought to determine, in a double-blind, placebo-controlled, randomized study, whether vitamin E supplementation (1,000 IU for three months) would improve impaired conduit and resistance vessel endothelial vasodilator function (EVF) and systemic arterial compliance (SAC) in type I diabetes mellitus (DM).
  
  
  BACKGROUND
  Oxidative stress is thought to be important in the pathogenesis of impaired EVF. Consistent with this hypothesis, we have recently shown that impaired EVF is related to low density lipoprotein (LDL) vitamin E content (VEC) in young subjects with type 1 DM.
  
  
  METHODS
  We assessed EVF in the brachial artery (using noninvasive ultrasound, flow-mediated vasodilation [FMD]; n = 41) and in the forearm resistance vessels (by flow responses to intrabrachial acetylcholine [ACh]; n = 21) and measured SAC (simultaneous aortic blood flow and carotid pressure measurements; n = 41) before and after active or placebo therapy.
  
  
  RESULTS
  The LDL VEC was increased by 127% after supplementation, resulting in a significant reduction in the oxidative susceptibility of LDL. There was no time-dependent change in FMD or in the response to ACh or SAC in the placebo group. A significant improvement in FMD (2.6 +/- 0.6% to 7.0 +/- 0.7%, p < 0.005) and the dose response to ACh (p < 0.05) were observed in those randomized to vitamin E therapy. Systemic arterial compliance was not affected by vitamin E (0.41 +/- 0.03 vs. 0.49 +/- 0.06 arbitrary compliance units, p = NS). The change in FMD was related to the change in LDL VEC (r = 0.42, p < 0.05) and the change in the oxidative susceptibility of LDL (r = 0.64, p < 0.0001).
  
  
  CONCLUSIONS
  Short-term daily oral supplementation with vitamin E improves EVF in both the conduit and resistance vessels of young subjects with type I DM.
authors.affiliation: Centre for Heart and Chest Research, Monash Medical Centre and Monash University, Melbourne, Australia.
authors.forename: R A
authors.initials: RA
authors.lastname: Skyrme-Jones
authors.forename: R C
authors.initials: RC
authors.lastname: O'Brien
authors.forename: K L
authors.initials: KL
authors.lastname: Berry
authors.forename: I T
authors.initials: IT
authors.lastname: Meredith
mesh_terms: D000284:Administration, Oral; D000328:Adult; D001783:Blood Flow Velocity / Q000187:drug effects; D001794:Blood Pressure; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000187:drug effects / Q000378:metabolism; D003187:Compliance / Q000187:drug effects; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D019587:Dietary Supplements; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D010991:Plethysmography; D016896:Treatment Outcome; D014463:Ultrasonography; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology; D014810:Vitamin E / Q000008:administration & dosage*
chemical_list: D008077:Lipoproteins, LDL; D014810:Vitamin E