Coenzyme Q10 and Obesity: An Overview

Trigeminal neuralgia (TN) is the neuropathic pain. Mitochondrial dysfunction, increased oxidative stress, and inflammation demonstrated in chronic pain. Carbamazepine (CBZ) is the first-line drug for TN, however, it is still insufficient. Coenzyme Q10 (CoQ10) has been used as the additional supplement for pain therapy. Nonetheless, mitochondrial respiratory proteins, oxidative stress, and inflammation in TN, and the add-on effects of CoQ10 on those defects have never been investigated. CBZ-treated TN-patients, naïve TN-patients, and control subjects were included. CBZ-treated TN-patients were randomised into two subgroups, received either CoQ10 or placebo for 2 months. Pain levels were evaluated, and peripheral blood mononuclear cells were isolated to determine the oxidative stress, mitochondrial oxidative phosphorylation (OXPHOS), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and cytokines including TNF-α, IL-1β and IL-18 mRNA expression. Pain scales, oxidative stress, and OXPHOS levels were greater in naïve TN-patients than control, whereas the cytokine profiles were unchanged. Although pain scales were lower in CBZ-treated TN-patients than in naïve TN-patients, oxidative stress, OXPHOS, and cytokine expression profiles were not different. PGC-1α levels found to be increased in CBZ-treated TN patients when compared with the naïve group. CoQ10 supplement in CBZ-treated TN patients reduced pain scale and oxidative stress and increased antioxidants levels when compared with placebo group. However, OXPHOS, PGC-1α, and cytokines were not different between groups. These findings suggest that increased oxidative stress could be potentially involved in the pathogenesis of TN. CoQ10 supplements can reduce oxidative stress, leading to more effective pain reduction in TN patients being treated with CBZ.

Nearly two thirds of the US population is overweight or obese and those numbers are climbing. Many organizations are beginning to recognize overweight and obesity as severe health threats and to acknowledge that treatment can serve as an important first step in addressing this epidemic. Through its Obesity with Co-morbidities Initiative, the Disease Management Association of America (DMAA) seeks to raise awareness and improve understanding of the role disease management (DM) can play in the treatment and management of obesity with comorbidities. Among the objectives of the Obesity with Co-morbidities Initiative was to develop standard definitions of obesity and obesity with comorbidities and to conduct qualitative research among key DM stakeholders. The first project undertaken and completed by the Obesity with Associated Co-morbidities Steering Committee and work group was to define the term "obesity" for consistent usage within the DM community for the purposes of population-based interventions. As part of this initiative, DMAA partnered with Synovate, a global market research firm, to conduct focus groups and in-depth interviews in order to collect qualitative data on attitudes and practices related to obesity treatment and coverage among key industry stakeholders, including health plans, disease management organizations, employers, and the business community. The findings indicated that obesity was widely recognized as a serious issue, but there remained varying opinions regarding responsibility, health and productivity costs, coverage, and best treatment methods among the participants. DMAA will continue this initiative through 2007 and will continue to develop a knowledge base of obesity guidelines and management practices, create valuable tools and resources including an online resource center, and facilitate partnerships with other organizations involved in the management and prevention of obesity.

BACKGROUND: According to the involvement of oxidative stress in the pathogenesis of obesity, the plasma level of coenzyme q10 in the correlation relationship with lipid metabolism disorders and functional liver state is of interest to study.AIM: Substantiation of approaches to the correction of lipid metabolism disorders and non-alcoholic fatty liver disease in children with exogenous obesity based on the content of coenzyme Q10 and its relationship with lipid profile and liver enzymes.MATERIALS AND METHODS: The single-center cross-sectional study enlisted the control (n=32, -1.0≤BMI SD score ≤+2.0) and obese (n=40, BMI SD score>+2.0) groups of children with the mean age of 12 yr. In all children BMI, lipidogram, liver enzymes (ALT and AST), plasma coenzyme Q10 and liver ultrasound examination were assessed.RESULTS: Patients of both groups were comparable (p> 0.05) in age and gender. The level of coenzyme Q10 in the compared groups was comparable (p> 0.05) and did not differ in patients with different degrees of obesity. According to the results of the study of the lipid profile in the obese children, the level of HDL was lower, and the level of LDL was higher than that in control group. The highest value of HDL was obtained in the patients with the 1st degree of obesity and the highest level of triglycerides — in the patients with the 4th degree of obesity. The control group demonstrated moderate correlations between endogenous coenzyme Q10 and total cholesterol (r=0.474, p=0.009) which persists in patients with the first degree of obesity (r = 0.548, p = 0.035). There was no difference in AST in the study groups, however, the main group demonstrated elevated ALT and ALT/AST ratio (p <0.001). The highest ALT and ALT / AST ratio were observed in patients with greatest degree of obesity. Eighteen obese children (45%) had ALT / AST ratio ≥1 (in the control group –one patient (3%) (p <0.001), while fourteen patients showed liver enlargement and structure change according to ultrasound (80%). The control group demonstrated moderate correlations between endogenous coenzyme Q10 and total cholesterol (r=0.474, p=0.009) and between coenzyme Q10 and ALT / AST ratio (r=0.412, p=0.023) . In the obese group there was correlation between AI and ALT / AST (r = 0.436, p = 0.006) and in patients with the 1st degree of obesity — between also coenzyme Q10 and ALT (r = 0.875, p <0.001).CONCLUSION: The disturbances in adequate control of cholesterol by coenzyme Q10 in obese children possibly confirming the involvement of oxidative stress in the pathogenesis of dyslipidemia and non-alcoholic fatty liver disease can serve as indication to use coenzyme Q10 in order to correct these complications.

The objective of this study was to examine the effects of coenzyme Q10 (CoQ10) supplementation on exercise-induced muscle damage and oxidative stress in sedentary young men. In this study, a total of 21 sedentary and healthy young men participated. Participants were assigned at random to a CoQ10 or a placebo group employing a double-blind method. Those in the CoQ10 group ingested 200 mg CoQ10 per day for 4 weeks. Those in the placebo group ingested the same dosage of a placebo. After the 4-week period, the same measurements and blood sampling were taken. At this point, eccentric exercise protocols (90° flexion and 180° extension, velocity 60°/s) were instigated for all subjects in isokinetic exercise dynamometry. After exercise, blood samples were taken immediately, 24, and 48 hours later. Blood samples were analyzed for plasma CoQ10 levels, serum creatine kinase (CK) activities, myoglobin (Mb) levels, plasma total superoxide dismutase (SOD) activities and malondialdehyde (MDA) levels. Plasma CoQ10 levels were higher in the CoQ10 supplemented group than in the placebo group (P<0.05). CK activities and levels of Mb increased in both groups 24 and 48 hours after exercise (P<0.05), but no significant difference between the groups was observed (P>0.05). Plasma total SOD activity and MDA levels were not significantly different in both groups 24 and 48 hours after exercise (P>0.05). CoQ10 supplementation does not prevent exercise induced muscle damage and oxidative stress in sedentary young men.

Mitochondria may be a principle source of oxidative stress causing MI/R injury. Coenzyme Q10 (CoQ10) is essential for electron transport in normal mitochondria, has antioxidant properties but its bioavailability is likely reduced due to oxidative stress during MI/R. Coenzyme Q1 (CoQ1) is a derivative of CoQ10, but is a more potent antioxidant than CoQ10 due to a shorter isoprene chain. We hypothesize that CoQ1 will exhibit better cardioprotective effects during MI/R. CoQ1 (MW=250 g/mol; 20 μM, n=4) and CoQ10 (MW=863 g/mol; 20 μM, n=5) were given at reperfusion in isolated rat hearts subjected to I (30 min)/R (45 min). We found that MI/R hearts (n=7) and MI/R+DMSO hearts (n=4) (1% DMSO was used to solubilize CoQ1 and CoQ10) exhibited significantly compromised cardiac contractile/diastolic pressures and coronary flow during reperfusion compared to those of sham hearts (n=5). By contrast, the final left ventricular developed pressure was significantly improved by CoQ1 treatment (53.5±5.5 mmHg), but not CoQ10 treatment (38.4±8.6 mmHg), when compared to that in MI/R hearts (33.6±6.2 mmHg) and MI/R+DMSO hearts (36.4±9.7 mmHg) (p&lt;0.05). Similarly, the final peak of the first derivative of left ventricular pressure was significantly higher in CoQ1 treatment (1180.2±103.0 mmHg/s), but not CoQ10 treatment (770.6±120.1 mmHg/s), when compared to that in MI/R hearts (700.6±134.7 mmHg/s) and MI/R+DMSO hearts (and 741.5±168.6 mmHg/s) (p&lt;0.05). CoQ1 and CoQ10 treated hearts showed no improvement on diastolic pressure and coronary flow compared to the controls. Moreover, infarct size was reduced by CoQ1 treatment (25±3%) and CoQ10 treatment (29±4%) compared to that in untreated MI/R (44±6%) and MI/R+DMSO (32±4%). In summary, our preliminary results indicate that CoQ1 was more effective than CoQ10 in restoring post‐reperfused cardiac contractile function, but not infarct size during MI/R.Support or Funding InformationThis study was supported by Division of Research, the Center for Chronic Disorders of Aging, and Department of Bio‐Medical Sciences at Philadelphia College of Osteopathic Medicine.

BackgroundIt has been reported that higher levels of oxidative stress and inflammation play a key role in the progression of hepatocellular carcinoma (HCC) after surgery. Coenzyme Q10 is an endogenous lipid-soluble antioxidant. To date, no intervention study has investigated coenzyme Q10 supplementation in HCC patients after surgery. The purpose of this study was to investigate oxidative stress, antioxidant enzymes activity, and inflammation levels in HCC patients after surgery following administration of coenzyme Q10 (300 mg/day).MethodsThis study was designed as a single-blinded, randomized, parallel, placebo-controlled study. Patients who were diagnosed with primary HCC (n = 41) and were randomly assign to a placebo (n = 20) or coenzyme Q10 (300 mg/day, n = 21) group after surgery. The intervention lasted for 12 weeks. Plasma coenzyme Q10, vitamin E, oxidative stress antioxidant enzymes activity and inflammatory markers levels were measured.ResultsThe oxidative stress (p = 0.04) and inflammatory markers (hs-CRP and IL-6, p < 0.01) levels were significantly decreased, and the antioxidant enzymes activity was significantly increased (p < 0.01) after 12 weeks of coenzyme Q10 supplementation. In addition, the coenzyme Q10 level was significantly negatively correlated with the oxidative stress (p = 0.01), and positively correlated with antioxidant enzymes activity (SOD, p = 0.01; CAT, p < 0.05; GPx, p = 0.04) and vitamin E level (p = 0.01) after supplementation.ConclusionIn conclusion, we demonstrated that a dose of 300 mg/d of coenzyme Q10 supplementation significantly increased the antioxidant capacity and reduced the oxidative stress and inflammation levels in HCC patients after surgery.Trial registrationClinical Trials.gov Identifier: NCT01964001

This article focuses on the hereditary ataxias, resulting from defects in specific genes, which include the spinocerebellar ataxias (SCAs), Friedreich's ataxia, and ataxia resulting from coenzyme Q10 (CoQ10) deficiency. CoQ10 is a vitamin-like substance that plays a key role in the biochemical process within mitochondria, supplying all cells with the energy required for normal functioning; CoQ10 is also important as an antioxidant, protecting cells (and particularly mitochondria) from free radical-induced oxidative damage. Oxidative stress, mitochondrial dysfunction and cellular energy depletion have been implicated in the pathogenesis of the hereditary ataxias; this provides a rationale for dietary supplementation with CoQ10 in these disorders. The authors have therefore reviewed clinical evidence for the potential benefit of oral supplementation with CoQ10 in the hereditary ataxias. Some categories of hereditary ataxia patients have demonstrated remarkable clinical improvement following CoQ10 supplementation, especially when administered at an early stage of disease. In particular, a number of studies have demonstrated significant symptomatic benefit in patients with ataxia resulting from primary CoQ10 deficiency, following oral supplementation with CoQ10. Although there is no consensus as to the dosage of CoQ10 to be used in ataxia management, clinical studies have typically used dosages in the range 300 to 3000 mg/day. With regard to safety, CoQ10 is generally well tolerated, with no significant adverse effects reported in long-term use.

Coenzyme Q10 is a fundamental endogenous factor involved in cell energy production that shows protective properties in oxidative stress, mainly in skeletal and heart muscle. Coenzyme Q10 supplementation appears to benefit athletes in strenuous training and in the elderly, demonstrating ant-inflammatory properties by reducing inflammatory cytokines. Improved absorption of coenzyme Q10 via a new delivery system would represent an important step forward in the use of coenzyme Q10 as a dietary supplement. The aim of the study was to evaluate the solubility and oral absorption in human healthy volunteers of a new food grade coenzyme Q10 phytosome formulation. Solubility studies were performed in vitro in simulated gastrointestinal fluids; human studies were conducted in healthy volunteers to evaluate oral absorption in a Single dose study, in comparison with the coenzyme Q10 capsules, and in a repeated study at two increasing doses. The highest solubility shown by coenzyme Q10 phytosome in simulated intestinal fluids results in an improvement in oral absorption of coenzyme Q10 in healthy volunteers, three times more than the coenzyme Q10 according to AUC (area under the time/concentration curve) values. When two increasing doses (one and two capsules) were administered to healthy volunteers within a two-week schedule, the plasmatic levels of coenzyme Q10 resulted in 0.864±0.200 μg/ml (Mean±S.D.+41%) and 1.321±0.400 μg/ml (+116%), respectively versus baseline (0.614±0.120 μg/ml one capsule, 0.614±0.160 μg/ml two capsules). This detected dose-related bioavailability of coenzyme Q10 phytosome was even observed with no alterations in vital signs, neither in the physical examination nor in ECG, and no changes of clinical and biochemical parameters were observed. These findings, taken together, support the safety profile and significantly improved coenzyme Q10 oral absorption in humans with this new phytosome delivery formulation.

Oral coenzyme Q10 supplementation improves clinical symptoms and recovers pathologic alterations in blood mononuclear cells in a fibromyalgia patient

The Complexities of Obesity

Mitochondria are primary targets for environmental toxic chemicals; these typically disrupt the mitochondrial electron transport chain, resulting in reduced ATP production, increased reactive oxygen free radical species (ROS)-induced oxidative stress, increased apoptosis, and increased inflammation. This in turn suggests a rationale for investigating the potential role of coenzyme Q10 (CoQ10) in mediating such chemical-induced mitochondrial dysfunction, given the key roles of CoQ10 in promoting normal mitochondrial function, and as an antioxidant and anti-apoptotic and anti-inflammatory agent. In the present article, we have, therefore, reviewed the potential role of supplementary CoQ10 in improving mitochondrial function and mediating adverse effects following exposure to a number of environmental toxins, including pesticides, heavy metals, industrial solvents, endocrine-disrupting agents, and carcinogens, as well as pharmacological drugs and lifestyle toxicants.

Coenzyme Q10 (CoQ10) is an essential cofactor in the mitochondrial electron transport chain and is found in all cell membranes. It is present in the body in both the reduced and oxidized forms, with the reduced form (CoQ10H2) having antioxidant properties. CoQ10 has been implicated in disease processes, including Parkinson disease (1), diabetes (2), and Alzheimer disease(3), as well as in aging (4), oxidative stress (4)(5), and hydroxymethylglutaryl-CoA reductase inhibitor (statin) therapy (6). In particular, changes in CoQ10 may be relevant to statin-induced myalgia (7). Generally the bioavailability of dietary CoQ10 is low, and the formulations of CoQ10 supplements affect bioavailability (8)(9). There is also a significant difference between individuals in absorption of CoQ10 from supplements (9). Knowledge of the biological variation of CoQ10 in healthy individuals enables interpretation of whether a significant change has occurred in response to a disease state or supplementation. We investigated the inter- and intraindividual variation of plasma total CoQ10, the ratio of total CoQ10 to LDL-cholesterol (LDL-C), and the ratio of total CoQ10 to total cholesterol (TC). Reference intervals for these variables in healthy New Zealand adults were also determined. For determination of the inter- and intraindividual variation of CoQ10, 10 healthy adult male volunteers were enrolled. Exclusion criteria included taking CoQ10 or other vitamin supplements, smoking, and use of any medications within 4 weeks before initiation of the study. All participants were self-reportedly healthy and disease free throughout the study. The median age of the participants was 23.5 (range, 21–28) years, the median weight was 69 (60–100) kg, and the median body mass index (BMI) was 21.4 (18.5–28.6) kg/m2. Blood samples were taken in the morning after …

Limited data are available indicating the effects of coenzyme Q10 (CoQ10) supplementation on metabolic status of patients with metabolic syndrome (MetS). The present study was conducted to determine the effects of CoQ10 administration on glucose homeostasis parameters, lipid profiles, biomarkers of inflammation and oxidative stress among patients with MetS. This randomized, double-blind, placebo-controlled trial was performed among 60 overweight or obese and type 2 diabetes mellitus patients with coronary heart disease aged 40-85years old. Participants were randomly allocated into two groups. Group A (n=30) received 100mg CoQ10 supplements and group B (n=30) received placebo for 8weeks. Fasting blood samples were taken at the beginning of the study and after 8-week intervention to quantify glucose homeostasis parameters, lipid profiles and biomarkers of inflammation and oxidative stress. Compared with the placebo, CoQ10 supplementation resulted in a significant reduction in serum insulin levels (-2.1±7.1 vs. +4.1±7.8µIU/mL, P=0.002) and homeostasis model of assessment-insulin resistance (-0.7±2.1 vs. +1.0±2.0, P=0.002) and homeostatic model assessment-beta cell function (-5.9±22.2 vs. +15.9±34.0, P=0.005). In addition, patients who received CoQ10 supplements had a significant increase in plasma total antioxidant capacity (TAC) concentrations (+26.0±105.0 vs. -162.2±361.8mmol/L, P=0.008) compared with the placebo group. However, after adjustment for the baseline levels, age and baseline BMI, the effect on TAC levels (P=0.08) disappeared. Additionally, compared with the placebo group, a significant positive trends in plasma glutathione (P=0.06) and a significant reduction in malondialdehyde (P=0.08) were seen among patients who received CoQ10 supplement. We did not observe any significant changes in fasting plasma glucose, lipid concentrations and inflammatory markers. Overall, daily intake of 100mg CoQ10 supplements among patients with MetS for 8weeks had beneficial effects on serum insulin levels, HOMA-IR, HOMA-B and plasma TAC concentrations. www.irct.ir : IRCT201502245623N35.

Bridges between mitochondrial oxidative stress, ER stress and mTOR signaling in pancreatic β cells

Introduction: Family physicians have an important role in the diagnosis and treatment of obesity, as most obese patients are first seen by the family physician.The aim of our study was to evaluate the obesity management of family physicians working in family heal th centers in Van province. Materials and Methods:This cross-sectional study was conducted between 04.05.2021-30.07.2021 with 126 volunteer family physicians working in family health centers representing Van province.The questionnaire including sociodemographic characteristics, obe sity knowledge and self-efficacy questions were completed by the physicians themselves.Results: Only 13 (10.3%) of the physicians knew the number of obese patients registered in their units.Although 97 (77%) of the physicians stated that the family physician was responsible for obesity management, 54 (42.9%) stated they calculated the body mass index of their patients "sometimes" and 48 (38.1%) "rarely".Seventy-one (56.3%) of the physicians thought family physicians had a great role in the prevention of obesity, while 63 (50%) argued the best role of the family physicians in obesity management isn't treating these patients but referring them to the relevant fields.Among physicians who calculated BMI "often", 6 6.7% indicated that they were professionally prepared to treat overweight patients and didn't consider themselves unsuccessful in getting their patients to lose weight. Conclusion:Our study shows that although obesity is included in chronic disease follow -up in primary care, it has not been put into practice.It is clear that there is a need to train family physicians on obesity management and to help them gain self -efficacy.