ubiquinone and Metabolic-Diseases

Although several trials have assessed the effect of coenzyme Q10 (CoQ10) supplementation on blood pressures among patients with metabolic diseases, findings are controversial.. This review of randomized controlled trials (RCTs) was performed to summarize the evidence on the effects of CoQ10 supplementation on blood pressures among patients with metabolic diseases.. Randomized-controlled trials (RCTs) published in PubMed, EMBASE, Web of Science and Cochrane Library databases up to 10 August 2017 were searched. Two review authors independently assessed study eligibility, extracted data, and evaluated risk of bias of included studies. Heterogeneity was measured with a Q-test and with I. A total of seventeen randomized controlled trials (684 participants) were included. Results showed that CoQ10 supplementation significantly decreased systolic blood pressure (SBP) (SMD - 0.30; 95% CI - 0.52, - 0.08). However, CoQ10 supplementation decreased diastolic blood pressure (DBP), but this was not statistically significant (SMD - 0.08; 95% CI - 0.46, 0.29).. CoQ10 supplementation may result in reduction in SBP levels, but did not affect DBP levels among patients with metabolic diseases. Additional prospective studies regarding the effect of CoQ10 supplementation on blood pressure in patients with metabolic diseases are necessary.

Topics: Adult; Aged; Blood Pressure; Dietary Supplements; Evidence-Based Medicine; Female; Humans; Hypertension; Male; Metabolic Diseases; Middle Aged; Odds Ratio; Randomized Controlled Trials as Topic; Risk Factors; Treatment Outcome; Ubiquinone

Oxidative stress and inflammation are key parameters in developing metabolic disorders. Hence, antioxidant intake might be an appropriate approach. Several studies have evaluated the effect of coenzyme Q10 (CoQ10) supplementation on lipid profile among patients with metabolic diseases, though findings are controversial. The aim of this systematic review and meta-analysis was to determine the effects of CoQ10 supplementation on lipid profile in patients with metabolic disorders.. We searched PubMed, EMBASE, Web of Science and Cochrane Library databases until July 2017. Prospective clinical trials were selected assessing the effect of CoQ10 supplementation on different biomarkers. Two reviewers independently assessed the eligibility of studies, extracted data, and evaluated the risk of bias of included studies. A fixed- or random-effects model was used to pool the data, which expressed as a standardized mean difference with 95% confidence interval. Heterogeneity was measured using a Q-test and with I2 statistics.. A total of twenty-one controlled trials (514 patients and 525 controls) were included. The meta-analysis indicated a significant reduction in serum triglycerides levels (SMD -0.28; 95% CI, -0.56, -0.005). CoQ10 supplementation also decreased total-cholesterol (SMD -0.07; 95% CI, -0.45, 0.31), increased LDL- (SMD 0.04; 95% CI, -0.27, 0.36), and HDL-cholesterol levels (SMD 0.10; 95% CI, -0.32, 0.51), not statistically significant.. CoQ10 supplementation may significantly reduce serum triglycerides levels, and help to improve lipid profiles in patients with metabolic disorders. Additional prospective studies are recommended using higher supplementation doses and longer intervention period.

Topics: Dietary Supplements; Humans; Lipids; Metabolic Diseases; Randomized Controlled Trials as Topic; Ubiquinone

Coenzyme Q (CoQ) is a vital component of the mitochondrial respiratory chain. A number of patients with CoQ deficiency presented with different clinical phenotypes, often affecting skeletal muscle, and responded well to CoQ supplementation. We discuss recent advances in this field with special attention to muscle involvement.. The identification of genetic defects causing CoQ deficiency has allowed to distinguish primary forms, due to mutations in biosynthetic genes, from secondary defects caused either by mutations in genes unrelated to CoQ biosynthesis or by nongenetic factors. To date, none of the patients with genetically proven primary deficiency presented with an exclusively (or prominently) myopathic phenotype. Most patients with myopathy were found to harbor other genetic defects (mutations in electron-transferring-flavoprotein dehydrogenase or mitochondrial DNA). The majority of patients with CoQ deficiency still lack a genetic diagnosis. The pathogenesis of CoQ deficiency cannot be attributed solely to the bioenergetic defect, suggesting that other roles of CoQ, including its antioxidant properties or its role in pyrimidine metabolism, may also play crucial roles.. Early recognition of CoQ deficiency is essential to institute appropriate and timely treatment, thus avoiding irreversible tissue damage.

Topics: Humans; Metabolic Diseases; Mitochondrial Myopathies; Muscle, Skeletal; Muscular Diseases; Ubiquinone

Huntington's disease (HD) is a neurodegenerative genetic disorder caused by an expansion of CAG repeats in the HD gene encoding for huntingtin (Htt), resulting in progressive death of striatal neurons, with clinical symptoms of chorea, dementia and dramatic weight loss. Metabolic and mitochondrial dysfunction caused by the expanded polyglutamine sequence have been described along with other mechanisms of neurodegeneration previously described in human tissues and animal models of HD. In this review, we focus on mitochondrial and metabolic disturbances affecting both the central nervous system and peripheral cells, including mitochondrial DNA damage, mitochondrial complexes defects, loss of calcium homeostasis and transcriptional deregulation. Glucose abnormalities have also been described in peripheral tissues of HD patients and in HD animal and cellular models. Moreover, there are no effective neuroprotective treatments available in HD. Thus, we briefly discuss the role of creatine and coenzyme Q10 that target mitochondrial dysfunction and impaired bioenergetics and have been previously used in HD clinical trials.

Topics: Animals; Creatine; Disease Models, Animal; Humans; Huntington Disease; Metabolic Diseases; Mitochondrial Diseases; Nerve Tissue; Ubiquinone

Topics: Antioxidants; Carotenoids; Coronary Disease; Humans; Lipid Peroxidation; Lipid Peroxides; Metabolic Diseases; Nutritional Requirements; Ubiquinone; Vitamin E

To evaluate the clinical symptoms and biochemical findings and establish the genetic etiology in a cohort of pediatric patients with combined deficiencies of the mitochondrial respiratory chain complexes.. Clinical and biochemical data were collected from 55 children. All patients were subjected to sequence analysis of the entire mitochondrial genome, except when the causative mutations had been identified based on the clinical picture. Whole exome sequencing/whole genome sequencing (WES/WGS) was performed in 32 patients.. Onset of disease was generally early in life (median age, 6 weeks). The most common symptoms were muscle weakness, hypotonia, and developmental delay/intellectual disability. Nonneurologic symptoms were frequent. Disease causing mutations were found in 20 different nuclear genes, and 7 patients had mutations in mitochondrial DNA. Causative variants were found in 18 of the 32 patients subjected to WES/WGS. Interestingly, many patients had low levels of coenzyme Q10 in muscle, irrespective of genetic cause.. Children with combined enzyme defects display a diversity of clinical symptoms with varying age of presentation. We established the genetic diagnosis in 35 of the 55 patients (64%). The high diagnostic yield was achieved by the introduction of massive parallel sequencing, which also revealed novel genes and enabled elucidation of new disease mechanisms.

Topics: Adolescent; Adult; Child; Child, Preschool; DNA Mutational Analysis; DNA, Mitochondrial; Exome Sequencing; Humans; Infant; Infant, Newborn; Metabolic Diseases; Mitochondrial Diseases; Mutation; Ubiquinone; Young Adult

Cancer development is mediated by oxidative stress and inflammation, which may correlate with metabolic disorders. The aim of this study was to evaluate antioxidant vitamins status and metabolic parameters in patients with oral cancer according to tumor-node-metastasis (TNM) stages.. A total of 194 patients with oral cancer were enrolled in this study. The patients were stratified for four groups according to cancer stages and that the statistics are comparisons across these groups. The levels of antioxidant vitamins (ubiquinone, β-carotene, vitamin A and E), metabolic parameters, oxidative stress, antioxidant enzymes activity, and inflammatory markers were measured.. More than half of the subjects had high blood pressure, central obesity, hyperglycemia, and hyperlipidemia regardless of TNM stage. With regard to antioxidant vitamins status, 46 and 94% of patients had β-carotene and ubiquinone deficiency, respectively. Patients in T3 and T4 stages had significantly lower antioxidant enzyme (catalase, p = 0.03) activity and higher inflammatory markers levels (high sensitivity C-reactive protein and interleukin-6, p < 0.01) than patients in the other stages. In addition, the level of β-carotene was negatively associated with waist circumference, and ubiquinone was positively associated with the level of high-density lipoprotein cholesterol (p < 0.05). Higher β-carotene and ubiquinone levels were negatively associated with hypertriglyceridemia and the risk of metabolic syndrome (p < 0.05).. A high proportion of patients with oral cancer had ubiquinone or β-carotene deficiency and metabolic disorders. The level of ubiquinone or β-carotene was negatively associated with the risk of central obesity, hypertriglyceridemia, and metabolic syndrome. Since patients with oral cancer suffer from high oxidative stress and inflammation (particularly in the T3 and T4 stages), supplementation with antioxidant vitamins such as ubiquinone or β-carotene could be preferentially applied.

Topics: Adult; Aged; beta Carotene; C-Reactive Protein; Cross-Sectional Studies; Female; Humans; Interleukin-6; Male; Metabolic Diseases; Middle Aged; Mouth Neoplasms; Neoplasm Staging; Oxidative Stress; Ubiquinone; Vitamin A; Vitamin E

Topics: Blood Pressure; Dietary Supplements; Humans; Metabolic Diseases; Randomized Controlled Trials as Topic; Ubiquinone

Topics: Alzheimer Disease; Anti-Inflammatory Agents, Non-Steroidal; Berberine; Humans; Inflammation; Metabolic Diseases; Selenium; Small Molecule Libraries; Ubiquinone; Vanadium Compounds

The specific activities of the succinate dehydrogenase-coenzyme Q reductase were assayed on mitochondrial preparations of this enzyme from spleen, liver, blood and peritoneal macrophages of mice infected with Friend leukemia virus, and of control mice. Significant increases in the deficiency of coenzyme Q-enzyme activity were found in the spleen and blood of infected animals as the infection progressed. No significant deficiency was observed in the liver or the peritoneal macrophages. The development of the deficiency and splenomegaly during infection seemingly correlate with previous data which showed that administration of coenzyme Q resulted in a reversal of splenomegaly and a reduction in mortality. A limiting factor in the resistance of mice to Friend leukemia virus appears to be the availability of coenzyme Q.

Topics: Animals; Friend murine leukemia virus; Leukemia, Experimental; Liver; Macrophages; Male; Metabolic Diseases; Mice; Peritoneal Cavity; Spleen; Succinate Dehydrogenase; Ubiquinone