Ubiquinol Ameliorates Endothelial Dysfunction in Subjects with Mild-to-Moderate Dyslipidemia: A Randomized Clinical Trial.

Jacopo Sabbatinelli,Roberta Galeazzi,Sonia Silvestri,Laura Mazzanti,Patrick Orlando,Phiwayinkosi V Dludla,Anna Rita Bonfigli,Roberto Antonicelli,Angelica Giuliani,Ilenia Cirilli,Fabiola Olivieri,Luca Tiano,Fabio Marcheggiani

doi:10.3390/nu12041098

Abstract

In this randomized, double-blind, single-center trial (ANZCTR number ACTRN12619000436178) we aimed to investigate changes in endothelium-dependent vasodilation induced by ubiquinol, the reduced form of coenzyme Q10 (CoQ10), in healthy subjects with moderate dyslipidemia. Fifty-one subjects with low-density lipoprotein (LDL) cholesterol levels of 130–200 mg/dL, not taking statins or other lipid lowering treatments, moderate (2.5%–6.0%) endothelial dysfunction as measured by flow-mediated dilation (FMD) of the brachial artery, and no clinical signs of cardiovascular disease were randomized to receive either ubiquinol (200 or 100 mg/day) or placebo for 8 weeks. The primary outcome measure was the effect of ubiquinol supplementation on FMD at the end of the study. Secondary outcomes included changes in FMD on week 4, changes in total and oxidized plasma CoQ10 on week 4 and week 8, and changes in serum nitrate and nitrite levels (NOx), and plasma LDL susceptibility to oxidation in vitro on week 8. Analysis of the data of the 48 participants who completed the study demonstrated a significantly increased FMD in both treated groups compared with the placebo group (200 mg/day, +1.28% ± 0.90%; 100 mg/day, +1.34% ± 1.44%; p < 0.001) and a marked increase in plasma CoQ10, either total (p < 0.001) and reduced (p < 0.001). Serum NOx increased significantly and dose-dependently in all treated subjects (p = 0.016), while LDL oxidation lag time improved significantly in those receiving 200 mg/day (p = 0.017). Ubiquinol significantly ameliorated dyslipidemia-related endothelial dysfunction. This effect was strongly related to increased nitric oxide bioavailability and was partly mediated by enhanced LDL antioxidant protection.

Highlights

Dyslipidemia, i.e., the alteration of one or more blood lipid fractions, including total cholesterol (TC), low-density lipoprotein (LDL)-cholesterol (LDL-C), triglycerides, and high-density lipoprotein (HDL)-cholesterol (HDL-C), is a major risk factor for cardiovascular disease (CVD) [1]
Premenopausal women were excluded due to their generally lower cardiovascular risk according to conventional algorithms [28], and to avoid any source of bias related to the high variability of flow-mediated dilation (FMD) during the different phases of the menstrual cycle [29]
The PP consisted of 48 subjects, 17 receiving ubiquinol 200 mg/day, 15 receiving ubiquinol

Summary

Introduction

Dyslipidemia, i.e., the alteration of one or more blood lipid fractions, including total cholesterol (TC), low-density lipoprotein (LDL)-cholesterol (LDL-C), triglycerides, and high-density lipoprotein (HDL)-cholesterol (HDL-C), is a major risk factor for cardiovascular disease (CVD) [1]. A well-established connection exists between cardiovascular risk factors, including dyslipidemia, endothelial dysfunction (ED), and atherosclerosis in the onset of cardiovascular disease [5,6]. The vascular endothelium plays a pivotal role in vascular homeostasis, sensing circulating signals that are capable of inducing phenotypic alterations of vessel walls and releasing a variety of autocrine and paracrine substances [7,8]. The shear stress exerted on the endothelium by flowing blood induces NO synthesis and release into the tunica media [11]

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