Coenzyme Q10 changes are associated with metabolic syndrome

Department of Mathematical Sciences, University of Cincinnati, Cincinnati, Ohio, United States
Clinica Chimica Acta (Impact Factor: 2.82). 07/2004; 344(1-2):173-9. DOI: 10.1016/j.cccn.2004.02.016
Source: PubMed


The purpose of this study was to determine whether coenzyme Q10 (CoQ) concentrations and redox status are associated with components of the metabolic syndrome.
This is a cross-sectional survey of 223 adults (28-78 years), who were drawn from the ongoing Princeton Follow-up Study in greater Cincinnati. Individuals were assessed for measures of fatness, blood pressure, glucose, lipid profiles, C-reactive protein (CRP), reduced CoQ (ubiquinol), oxidized CoQ (ubiquinone), total CoQ and CoQ redox ratio (ubiquinol/ubiquinone).
After adjusting for age, sex and race, we found that total CoQ, ubiquinol and CRP levels are significantly increased in metabolic syndrome. Comparison of minimal risk and high-risk metabolic syndrome groups indicates an increased CoQ redox ratio in the high risk group (p<0.05). Step-wise logistic regression analysis, using age, sex, race, (ln)CRP, total cholesterol, LDL, ubiquinol, ubiquinone and total CoQ as predictors, shows that only age (p=0.001), total CoQ adjusted for plasma lipids (p<0.0001) and (ln)CRP (p<0.005) were significant predictors of metabolic syndrome.
The presence of metabolic syndrome components are associated with increased plasma total CoQ and ubiquinol concentrations after adjusting for age, sex and race. An increase in CoQ redox ratio may indicate a gender-specific adaptive response to oxidative stress in females, but not males.

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    • "The latter function seems to be important for inflammatory processes [9], aging [6], cholesterol metabolism [6], and erythropoiesis [8]. The CoQ 10 status in humans seems to be an important risk factor for several diseases including heart failure [10] [11] [12] [13], atherosclerosis [14] [15] [16], or the metabolic syndrome [17]. Recently, Mortensen et al. published the results from Q-SYMBIO, an international, randomized, double-blind multicenter intervention study with CoQ 10 supplementation in 420 patients with chronic heart failure [18]. "
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    ABSTRACT: Coenzyme Q10 (CoQ10 ) exists in a reduced (ubiquinol) and an oxidized (ubiquinone) form in all human tissues and functions, amongst others, in the respiratory chain, redox-cycles, and gene expression. As the status of CoQ10 is an important risk factor for several diseases, here we determined the CoQ10 status (ubiquinol, ubiquinone) in a large Caucasian study population (n = 1,911). The study population covers a wide age range (age: 18-83 years, 43.4% men), has information available on more than 10 measured clinical phenotypes, more than 30 diseases (presence vs. absence), about 30 biomarkers, and comprehensive genetic information including whole-genome SNP typing (>891,000 SNPs). The major aim of this long-term resource in CoQ10 research is the comprehensive analysis of the CoQ10 status with respect to integrated health parameters (i.e., fat metabolism, inflammation), disease-related biomarkers (i.e., liver enzymes, marker for heart failure), common diseases (i.e., neuropathy, myocardial infarction), and genetic risk in humans. Based on disease status, biomarkers, and genetic variants, our cohort is also useful to perform Mendelian randomisation approaches. In conclusion, the present study population is a promising resource to gain deeper insight into CoQ10 status in human health and disease. © 2015 BioFactors, 2015. © 2015 International Union of Biochemistry and Molecular Biology.
    No preview · Article · Jul 2015 · BioFactors
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    • "Recent studies have provided beneficial effects of CoQ10 in various disorders related to oxidative stress like hypertension and heart failure.(23–25) It has been reported that CoQ10 concentrations and redox status are associated with components of MS.(26) "
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    ABSTRACT: This study was conducted to investigate the effects of alpha-lipoic acid and coenzyme Q10 on plasma levels of lipids, asymmetric dimethylarginine, oxidative stress in fructose fed rats which provide a model of dietary-induced insulin resistance and to evaluate vascular changes developing in these rats by histologically. Male Sprague Dawley rats were used in this study. The animals were divided into 4 groups. Group 1 did not receive any medication and served as a control. Group 2 received a regular diet and water ad libitum and fructose was administered as % 10 solution in drinking water. Group 3 received alpha-lipoic acid (100 mg/kg/day) i.p. for 5 weeks and Group 4 received coenzyme Q10 (10 mg/kg/day) i.p. for 5 weeks. For determination of plasma asymmetric dimethylarginine, glutathione and malondialdehyde levels, high-performance liquid chromatography system was used. Homeostatic model assessment as a measure of insulin resistance was calculated. Lipid profile measurements were determined using enzymatic assay on an Auto analyzer. The high fructose diet was significantly associated with an increase in levels of plasma LDL, VLDL and total cholesterol and decrease in level of HDL cholesterol. Plasma asymmetric dimethylarginine, malondialdehyde and glutathione levels were also increase in these rats. alpha-lipoic acid or coenzyme Q10 supplementation was found to have some positive effect on these parameters. These findings were also demonstrated by morphological observation of the aorta. We demonstrated that administration of alpha-lipoic acid and coenzyme Q10 notably suppresses oxidative and nitrative stress, hyperinsulinemia, insulin resistance developing in fructose fed rats, a model of metabolic syndrome (MS). These positive effects of alpha-lipoic acid or coenzyme Q10 can be attributed to its antioxidant activity.
    Preview · Article · Mar 2012 · Journal of Clinical Biochemistry and Nutrition
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    ABSTRACT: The present study examines the influence of menopause and hormone replacement therapy (HRT) on serum levels of coenzyme Q(10) and other lipid-soluble antioxidants in normal women. Serum levels of coenzyme Q(10), alpha-tocopherol, gamma-tocopherol, beta-carotene and lycopene in 50 premenopausal women (not using oral contraceptives), 33 healthy postmenopausal and 15 postmenopausal women on HRT ("Prempo"; combination of 0.625 mg conjugated estrogen and 2.5 mg medroxyprogesterone acetate) were measured by high-pressure liquid chromatography. Lipid profiles were also analyzed. Significantly higher serum coenzyme Q(10) and alpha-tocopherol levels were detected in postmenopausal compared with premenopausal women (P < 0.05, and < 0.001); whereas, in postmenopausal subjects on HRT, we detected a significant decrease in coenzyme Q(10) and gamma-tocopherol levels (P < 0.001, and < 0.05) and increased alpha-tocopherol levels (P < 0.05). Serum levels of beta-carotene, lycopene, LDL, HDL, cholesterol and triglyceride were comparable among the study groups. Coenzyme Q(10) is postulated to be involved in preventing cardiovascular disease (CVD) because of its bioenergetics role in the mitochondrial respiratory chain and its antioxidant properties at the mitochondrial and extramitochondrial levels. The decrease in serum concentrations of coenzyme Q(10), produced by HRT, may promote oxygen free radical-induced membrane damage and may, thus alter cardiovascular risk in postmenopausal women. HRT-induced reductions in lipid-soluble antioxidant(s) levels, and its potential consequences on CVD, needs to be further investigated.
    No preview · Article · Jan 2005 · BioFactors
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