Watts GF, Playford DA, Croft KD, Ward NC, Mori TA, Burke V. Coenzyme Q(10) improves endothelial dysfunction of the brachial artery in type II diabetes mellitus

Department of Medicine, University of Western Australia, Royal Perth Hospital, Perth, Australia.
Diabetologia (Impact Factor: 6.67). 04/2002; 45(3):420-6. DOI: 10.1007/s00125-001-0760-y
Source: PubMed


We assessed whether dietary supplementation with coenzyme Q(10) improves endothelial function of the brachial artery in patients with Type II (non-insulin-dependent) diabetes mellitus and dyslipidaemia.
A total of 40 patients with Type II diabetes and dyslipidaemia were randomized to receive 200 mg of coenzyme Q(10) or placebo orally for 12 weeks. Endothelium-dependent and independent function of the brachial artery was measured as flow-mediated dilatation and glyceryl-trinitrate-mediated dilatation, respectively. A computerized system was used to quantitate vessel diameter changes before and after intervention. Arterial function was compared with 18 non-diabetic subjects. Oxidative stress was assessed by measuring plasma F(2)-isoprostane concentrations, and plasma antioxidant status by oxygen radical absorbance capacity.
The diabetic patients had impaired flow-mediated dilation [3.8 % (SEM 0.5) vs 6.4 % (SEM 1.0), p = 0.016], but preserved glyceryl-trinitrate-mediated dilation, of the brachial artery compared with non-diabetic subjects. 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.
Coenzyme Q(10) supplementation improves endothelial function of conduit arteries of the peripheral circulation in dyslipidaemic patients with Type II diabetes. The mechanism could involve increased endothelial release and/or activity of nitric oxide due to improvement in vascular oxidative stress, an effect that might not be reflected by changes in plasma F(2)-isoprostane concentrations.

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Available from: David Playford, May 18, 2015
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    • "It has also been reported that CoQ10 is significantly low in mitochondria of Parkinson patients (Shults, 2005). In clinical studies, CoQ10 has been used to improve sperm immobility, endothelial dysfunctions and in type 2 diabetic patients (Balercia et al., 2002; Hodgson et al., 2002; Mancini et al., 1994; Playford et al., 2003; Watts et al., 2002). The MPTP is a non-specific channel in the inner mitochondrial membrane for transferring small molecules. "
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    ABSTRACT: CoQ10 shares a biosynthetic pathway with cholesterol therefore it can be a potential target of the widely available lipid-lowering agents such as statins. Statins are the most widely prescribed cholesterol-lowering drugs with the ability to inhibit HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductase. Preclinical and clinical safety data have shown that statins do not cause serious adverse effects in humans. However, their long-term administration is associated with a variety of myopatic complaints. The aim of this study was to investigate whether CoQ10 supplementation of animals under high fat diet (HFD) treated with statins is able to bypass the mitochondrial metabolic defects or not? Animals were divided into 7 groups and fed with either regular (RD) or HFD during experiments. The first group considered as regular control and fed with a RD. Groups 2-7 including HFD control, CoQ10 (10 mg/kg), simvastatin (30 mg/kg), atorvastatin (30 mg/kg), simvastatin+ CoQ10 or atorvastatin+ CoQ10 treated orally for 30 days and fed with HFD. At the end of treatments, the animals were killed and blood samples were collected for biochemical examinations. The rat liver mitochondria were isolated and several mitochondrial indices including succinate dehydrogenase activity (SDA), ATP levels, mitochondrial membrane potential (MMP) and mitochondrial permeability transition pore (MPP) were determined. We found that triglyceride (Tg), cholesterol (Chol) and low-density lipoprotein (LDL) were augmented with HFD compared to RD and treatment with statins remarkably lowered the Tg, Chol and LDL levels. Mitochondrial parameters including, SDA, ATP levels, MMP and MPP were reduced with statin treatment and improved by co-administration with CoQ10.
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    • "One study also compared CoQ 10 stand-alone treatment to a CoQ 10 -fenofibrate combination and to fenofibrate (a lipid-lowering medication) alone. Primary outcomes were endothelial function of the brachial artery [Watts et al., 2002], blood pressure [Hodgson et al., 2002], glycemic control [Hodgson et al., 2002], and forearm microcirculatory function [Playford et al., 2003]. CoQ 10 supplementation in this population raised plasma CoQ 10 levels, improved endothelial function in the brachial artery , significantly decreased both systolic and diastolic blood pressure, decreased glycosylated hemoglobin (HbA1C), and, in combination with fenofibrate, markedly improved both endothelial and non-endothelial forearm vasodilation. "
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    ABSTRACT: For a number of years, coenzyme Q10 (CoQ10) was known for its key role in mitochondrial bioenergetics; later studies demonstrated its presence in other subcellular fractions and in blood plasma, and extensively investigated its antioxidant role. These two functions constitute the basis for supporting the clinical use of CoQ10. Also at the inner mitochondrial membrane level, CoQ10 is recognized as an obligatory co-factor for the function of uncoupling proteins and a modulator of the mitochondrial transition pore. Furthermore, recent data indicate that CoQ10 affects expression of genes involved in human cell signalling, metabolism, and transport and some of the effects of CoQ10 supplementation may be due to this property. CoQ10 deficiencies are due to autosomal recessive mutations, mitochondrial diseases, ageing-related oxidative stress and carcinogenesis processes, and also statin treatment. Many neurodegenerative disorders, diabetes, cancer and muscular and cardiovascular diseases have been associated with low CoQ10 levels, as well as different ataxias and encephalomyopathies. CoQ10 treatment does not cause serious adverse effects in humans and new formulations have been developed that increase CoQ10 absorption and tissue distribution. Oral CoQ10 is a frequent antioxidant strategy in many diseases that may provide a significant symptomatic benefit.
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    • "It is a more powerful antioxidant than vitamin E, so it can neutralise tocopheroxyl radicals and regenerates its reduced form (Nagaoka et al., 2000). Its beneficial effects have been shown in diabetes mellitus, hypercholesterolaemia , hypertension, neurodegenerative diseases and lipid peroxidation (Leibovitz et al., 1990; Watts et al., 2002; Shults et al., 2002; Rosenfeldt et al., 2007; Hamilton et al., 2009; ). Besides, its deficiency has been found in infertile men with sperm disorders (Mancini et al., 1998, 2005). "
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