Effect of oral vitamin E (α‐tocopherol) supplementation on vascular endothelial function in Type 2 diabetes mellitus

Abstract

There may be receptor-specific endothelial dysfunction in subjects with uncomplicated Type 2 DM. This is not improved by treatment with alpha-tocopherol.

Coenzyme Q10 improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus

“…There is evidence in Type II diabetes for and against improvement in vasodilator function of forearm resistance arteries in response to the muscarinic agonist acetylcholine with vitamin E supplementation [10,11]. One positive study using a vitamin E analogue was not placebo controlled but did show reduction in plasma F 2 -isoprostanes in a small number of patients [11].…”

“…One positive study using a vitamin E analogue was not placebo controlled but did show reduction in plasma F 2 -isoprostanes in a small number of patients [11]. Vitamin E supplementation was reported to improve forearm microcirculatory function in a larger sample of Type II diabetic patients in a well-controlled trial [10]. Improvement in methacholine-mediated vasodilator function of forearm resistance vessels was also reported in Type II diabetes following the intra-arterial administration of vitamin C [12].…”

“…Flow-mediated dilation of the brachial artery increased by 1.6 % (SEM 0.3) with coenzyme Q 10 and decreased by ±0.4 % (SEM 0.5) with placebo (p = 0.005); there were no group differences in the changes in pre-stimulatory arterial diameter, post-ischaemic hyperaemia or glyceryl-trinitrate-mediated dilation response. Coenzyme Q 10 treatment resulted in a threefold increase in plasma coenzyme Q 10 (p < 0.001) but did not alter plasma F 2 -isoprostanes, oxygen radical absorbance capacity, lipid concentrations, glycaemic control or blood pressure.…”

Endothelial dysfunction in diabetes

“…This may be related to the more limited contribution of NO to endothelium-dependent vasodilatation in these vessels. In the forearm circulation of patients with type II diabetes, vitamin E supplementation during 8 weeks did not improve endothelium-dependent vasodilatation (Gazis et al, 1999). Surprisingly, high dose vitamin E supplementation caused a further attenuation of endothelium-dependent vasodilatation in mesenteric arteries of the rat, despite a decrease of the 8-epi-prostaglandin F 2a level, an indicator of oxidative stress (Palmer et al, 1998a), suggesting that exaggerated antioxidant supplementation may even be deleterious.…”

“…Impaired ACh-induced relaxation with normal responses to bradykinin has been reported in isolated resistance vessels from patients with type I diabetes (McNally et al, 1994), in the forearm circulation of type II diabetes patients (Gazis et al, 1999) and in mesenteric and hindlimb arteries of streptozotocin (STZ)-rats (Lash & Bohlen, 1991;Taylor et al, 1995), suggesting an abnormality at the level of the G-proteins. However, several other studies found equally suppressed responses to di erent endothelium-dependent agonists (Heygate et al, 1995;Fulton et al, 1996;Costa e Forti & Fonteles, 1998;Mayhan & Patel, 1995;1998;Mayhan, 1997) or impaired relaxation to the calcium-ionophore A23187 (Oyama et al, 1986;Durante et al, 1988;Cameron & Cotter, 1992;Fukao et al, 1997), making a disturbance of receptors or receptor-coupled mechanisms unlikely as a common mechanism of endothelial dysfunction.…”