ubiquinone and Diabetes-Mellitus

Coenzyme Q10 (CoQ10) has been known as ubiquinone or ubidecarenone, which is a kind of lipid-soluble and vitamin-like antioxidant. It has a potent antioxidant effect against oxidation status via various mechanisms, including its ability to regenerate other antioxidants, such as vitamin E and vitamin C, and to increase antioxidant enzymes. Moreover, CoQ10 can quench free radicals and prevent lipid peroxidation. The aim of this systematic review and meta-analysis was to evaluate the effect of CoQ10 on oxidative stress variables.. A comprehensive electronic database search in Scopus, Web of Science, Embase, Cochrane Library, and Medline was performed to identify eligible randomized clinical trials. A meta-analysis of included studies was performed on selected variables using a random-effects model. Quality assessment was conducted by means of the Cochrane risk of bias assessment tool.. To evaluate the effect of CoQ10 supplementation, 17 trials and 972 participants were included for the meta-analysis. The pooled analysis of primary studies showed that CoQ10 increased serum total antioxidant capacity (standardized mean difference [SMD] 0.62 mmol/L, 95% CI 0.18-1.05, I2 = 76.1%, p ˂ 0.001) and superoxide dismutase (SMD 0.40 U/mg, 95% CI 0.12-0.67, I2 = 9.6%, p ˂ 0.345) levels and decreased malondialdehyde (SMD -1.02 mmol/L, 95% CI -1.60 to -0.44, I2 = 88.2%, p ˂ 0.001) level significantly compared to the placebo group. Although the effect of CoQ10 on nitric oxide (SMD 1.01 µmol/L, 95% CI -1.53 to 3.54, p ˂ 0.001, I2 = 97.8%) and glutathione peroxidase (SMD -0.01 mmol/L, 95% CI -0.86 to 0.84, p ˂ 0.001, I2 = 88.6%) was not significant, CoQ10 can be mentioned as an improvement in antioxidant defense status against reactive oxygen species.. These supplements have positive effects on antioxidant defense against oxidizing agents and elevate antioxidant enzyme levels in the body. However, due to limited research the results should be taken with caution.. Hintergrund: Coenzym Q10 (CoQ10) ist als Ubichinon oder Ubidecarenon bekannt; dies ist ein Gruppe fettlöslicher, vitaminähnlicher Antioxidantien. Es wirkt als starkes Antioxidans auf den Oxidationsstatus. Diese Wirkung beruht auf mehreren Mechanismen, darunter seiner Fähigkeit zur Regeneration anderer Antioxidantien wie z. B. Vitamin E und Vitamin C sowie zur Förderung antioxidativer Enzyme. Darüber hinaus vermag CoQ10 freie Radikale einzufangen und die Lipidperoxidation zu verhindern. Das Ziel dieser systematischen Übersichtsarbeit und Metaanalyse war es, die Auswirkungen von CoQ10 auf verschiedene Parameter des oxidativen Stress zu untersuchen. Methoden: Eine umfassende Suche in den elektronischen Datenbanken Scopus, Web of Science, Embase, Cochrane Library und Medline wurde durchgeführt, um randomisierte klinische Studien zu finden, die unseren Anforderungen entsprachen. Eine Metaanalyse der eingeschlossenen Studien wurde bei ausgewählten Variablen mit einem Random-Effects-Modell durchgeführt. Die Beurteilung der Qualität erfolgte mit dem Risk-of-Bias-Tool von Cochrane. Ergebnisse: Um die Auswirkungen der Supplementierung von CoQ10 zu untersuchen, wurden 17 Studien mit 972 Teilnehmern in die Metaanalyse eingeschlossen. Die aggregierte Analyse der Primärstudien ergab, dass CoQ10 im Vergleich zu Placebo die Serumwerte für antioxidative Gesamtkapazität (standardisierte mittlere Differenz [SMD] 0,62 mmol/L, 95%-KI 0,18–1,05, I2 = 76,1%, p ˂ 0,001) und Superoxid-Dismutase (SMD 0,40 U/mg, 95%-KI 0,12–0,67, I2 = 9,6%, p ˂ 0,345) erhöhte und die für Malondialdehyd (SMD –1,02 mmol/L, 95%-KI –1,60 bis –0,44, I2 = 88,2%, p ˂ 0,001) senkte, jeweils in signifikantem Maße. Der Effekt von CoQ10 auf Stickstoffmonoxid (SMD 1,01 µmol/L, 95%-KI –1,53 bis 3,54, p ˂ 0,001, I2 = 97,8%) und Glutathionperoxidase (SMD –0,01 mmol/L, 95%-KI –0,86 bis 0,84, p ˂ 0,001, I2 = 88,6%) war hingegen nicht signifikant. CoQ10 kann eine Verbesserung des Status der antioxidativen Abwehr gegen reaktive Sauerstoffspezies bewirken. Schlussfolgerung: Die Supplementierung wirkt sich positiv auf die antioxidative Abwehr gegen oxidierende Substanzen aus und erhöht die im Körper vorliegende Konzentration antioxidativer Enzyme. Angesichts der Beschränkungen einiger der Studien sind diese Ergebnisse jedoch mit Vorsicht zu interpretieren.

Topics: Age Factors; Diabetes Mellitus; Dietary Supplements; Humans; Oxidative Stress; Ubiquinone

This review examines recent randomized clinical trials evaluating the role of coenzyme Q10 (CoQ10) in the management of coronary heart disease.. CoQ10 is one of the most commonly used dietary supplements in the USA. Due to its antioxidant and anti-inflammatory effects, CoQ10 has been studied extensively for possible use in managing coronary heart disease. One of the most common applications of CoQ10 is to mitigate statin-associated muscle symptoms (SAMS) based on the theory that SAMS are caused by statin depletion of CoQ10 in the muscle. Although previous studies of CoQ10 for SAMS have produced mixed results, CoQ10 appears to be safe. Because CoQ10 is a cofactor in the generation of adenosine triphosphate, supplementation has also recently been studied in patients with heart failure, which is inherently an energy deprived state. The Q-SYMBIO trial found that CoQ10 supplementation in patients with heart failure not only improved functional capacity, but also significantly reduced cardiovascular events and mortality. Despite these positive findings, a larger prospective trial is warranted to support routine use of CoQ10. Less impressive are the effects of CoQ10 on specific cardiovascular risk factors such as blood pressure, dyslipidemia, and glycemic control. Current evidence does not support routine use of CoQ10 in patients with coronary heart disease. Additional studies are warranted to fully determine the benefit of CoQ10 in patients with heart failure before including it in guideline-directed medical therapy.

Topics: Antioxidants; Blood Glucose; Cardiovascular Diseases; Chronic Disease; Coronary Disease; Diabetes Mellitus; Dietary Supplements; Dyslipidemias; Heart Failure; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypertension; Muscular Diseases; Randomized Controlled Trials as Topic; Risk Factors; Ubiquinone

CoenzymeQ10 (CoQ10 ), or ubiquinone, is an endogenous enzyme cofactor produced by most human cells. It is a potent antioxidant and is necessary for energy production in mitochondria. Diabetes mellitus is a chronic disease with multiple metabolic abnormalities, principally resulting from the inflammation and oxidative stress associated with mitochondrial dysfunctions. Clinical trials of the effects of supplementary CoQ10 on metabolic control in diabetes have reported inconsistent results. We undertook a systematic review and meta-analysis of randomized controlled trials to assess the effects of CoQ10 supplementation on glycaemic control, lipid profile and blood pressure in patients with diabetes.. A systematic search was conducted on MEDLINE, The Cochrane Library, CINAHL, NCCAM, Web of Science, Scopus, ClinicalTrials.gov and historical search of reference lists of relevant articles. The bibliographic databases were searched from inception to February 2015. We included randomized, placebo-controlled trials of CoQ10 in diabetes lasting at least 12 weeks. HbA1c or fasting plasma glucose had to be reported. Primary outcome was glycemic control, and secondary outcomes were lipid profile and blood pressure. Treatment effect was estimated with mean difference.. Seven trials were included in the meta-analysis, involving 356 patients. Neither CoQ10 alone nor CoQ10 plus fenofibrate improved glycemic control. In addition, CoQ10, alone or in combination with fenofibrate, did not alter LDL-C, HDL-C and blood pressure. Triglycerides levels were significantly reduced with CoQ10 (mean difference -0·26 mmol/L, 95% CI -0·05 mmol/L to -0·47 mmol/L, P = 0·02) and CoQ10 plus fenofibrate (mean difference -0·72 mmol/L, 95% CI -0·32 mmol/L to -1·12 mmol/L, P = 0·0004). CoQ10 plus fenofibrate also effectively reduced total cholesterol (mean difference: -0·45 mmol/L, 95% CI -0·06 mmol/L to -0·84 mmol/L, P = 0·02).. CoQ10 supplementation has no beneficial effects on glycemic control, lipid profile or blood pressure in patients with diabetes. However, it may reduce triglycerides levels. Due to limited data availability, well-powered and well-designed randomized controlled trials are needed to clearly determine the effect of CoQ10 on metabolic profile in diabetes. Dosage effects should also be explored.

Topics: Antioxidants; Blood Glucose; Blood Pressure; Diabetes Mellitus; Dietary Supplements; Humans; Lipids; Randomized Controlled Trials as Topic; Ubiquinone; Vitamins

New-onset diabetes has been observed in clinical trials and meta-analyses involving statin therapy. To explain this association, three major mechanisms have been proposed and discussed in the literature. First, certain statins affect insulin secretion through direct, indirect or combined effects on calcium channels in pancreatic β-cells. Second, reduced translocation of glucose transporter 4 in response to treatment results in hyperglycemia and hyperinsulinemia. Third, statin therapy decreases other important downstream products, such as coenzyme Q10, farnesyl pyrophosphate, geranylgeranyl pyrophosphate, and dolichol; their depletion leads to reduced intracellular signaling. Other possible mechanisms implicated in the effect of statins on new-onset diabetes are: statin interference with intracellular insulin signal transduction pathways via inhibition of necessary phosphorylation events and reduction of small GTPase action; inhibition of adipocyte differentiation leading to decreased peroxisome proliferator activated receptor gamma and CCAAT/enhancer-binding protein which are important pathways for glucose homeostasis; decreased leptin causing inhibition of β-cells proliferation and insulin secretion; and diminished adiponectin levels. Given that the magnitude of the risk of new-onset diabetes following statin use remains to be fully clarified and the well-established beneficial effect of statins in reducing cardiovascular risk, statins remain the first-choice treatment for prevention of CVD. Elucidation of the mechanisms underlying the development of diabetes in association with statin use may help identify novel preventative or therapeutic approaches to this problem and/or help design a new generation statin without such side-effects.

Topics: Adipocytes; Adiponectin; Animals; Calcium Channels; Caveolins; Cell Differentiation; Diabetes Mellitus; Dolichols; Glucose Transporter Type 4; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hyperglycemia; Hyperinsulinism; Insulin; Insulin Resistance; Insulin Secretion; Insulin-Secreting Cells; Ion Channels; Leptin; MicroRNAs; Mitochondrial Proteins; Terpenes; Ubiquinone; Uncoupling Protein 3

Statins are drugs with the unquestionable effectiveness in the reduction of low density lipoprotein cholesterol (LDL-C) and the cardiovascular risk with the acceptable safety profile. On the basis of the above statins are the most common used drugs worldwide. The present review is aimed to discuss the potential mechanisms of statins leading to occurrence of glucose metabolism disturbances through the influence on insulin secretion by the beta-cells of pancreatic islets and the cells' sensitivity on insulin. It might be a results of disadvantageous statin properties connected to the intensification of inflammation and oxidation within the pancreatic islets, and the influence on adipokines secretion by the fat tissue cells. However, it should be emphasized that despite the recommendations of US Food and Drug Administration suggesting to keep caution in connection to potentially prodiabetic statins' properties, this data need to be confirmed in large multicenter clinical trials with properly designed main endpoints.

Topics: Adipokines; Adipose Tissue; Cholesterol, LDL; Diabetes Mellitus; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Insulin; Insulin Resistance; Insulin Secretion; Insulin-Secreting Cells; Pancreatitis; Ubiquinone

Diabetes is a chronic metabolic disorder that continues to present as a major health problem worldwide. It is characterized by absolute or relative deficiencies in insulin secretion and/or insulin action and is associated with chronic hyperglycemia and disturbances of carbohydrate, lipid, and protein metabolism. Many studies suggest a central role for oxidative stress in the pathogenesis of this multi-faceted metabolic disorder. This has prompted investigations in the use of antioxidants as a complementary therapeutic approach. In this review we briefly summarize oxidative mechanisms implicated in diabetic complications and then focus on the findings resulting from human clinical trials where antioxidants were studied as an adjuvant to standard diabetes treatment during the last ten years. A literature search using PubMed (last ten years) was performed using the following terms: vitamin E, vitamin C, coenzyme Q10, alpha lipoic acid, L-carnitine, ruboxistaurin or LY 333531 and diabetes. This search was limited to human clinical trials. We concluded there is not any established benefit for antioxidants use in the management of diabetic complications. Therefore, routine vitamin or mineral supplementation is not generally recommended.

Topics: Antioxidants; Ascorbic Acid; Carnitine; Clinical Trials as Topic; Diabetes Complications; Diabetes Mellitus; Diabetes Mellitus, Type 2; Female; Humans; Indoles; Male; Maleimides; Oxidative Stress; Thioctic Acid; Treatment Outcome; Ubiquinone; Vitamins

Reactive oxygen species (ROS) have deleterious or beneficial effects; this dual nature of ROS means that ROS act as intracellular signaling molecules and as defense mechanisms against micro-organisms. An overproduction of ROS results in oxidative stress, a deleterious process that damages cell structures, including lipids, proteins, and DNA. Oxidative stress plays a major role in various human disease states, including endocrine dysfunction. As a safeguard against oxidative stress, several endogenous nonenzymatic and enzymatic antioxidant systems exist. Antioxidants can delay or prevent oxidative stress and are widely used in the hope of maintaining health and preventing diseases. Although early studies suggested that antioxidant supplements promoted health, later clinical trials revealed that it may not be true in all cases. In this article, we provide a brief review of the pathophysiologic aspects of oxidative stress in a number of the most commonly human endocrionopathies (diabetes, male and female infertility and thyroid diseases) and review the therapeutic potentials of existing antioxidant strategies. We focus on human clinical trials and discuss the implications of their results. Based on the data reported so far, we conclude that the results reported challenge us to design better antioxidant trials in future, with a particular emphasis on identifying 1) appropriate doses 2) selecting the right populations 3) treating for optimal durations and 4) specific intracellular targeting mechanisms.

Topics: Antioxidants; Ascorbic Acid; Diabetes Mellitus; Female; Humans; Infertility; Male; Oxidative Stress; Reactive Oxygen Species; Thioctic Acid; Thyroid Diseases; Ubiquinone; Vitamin E

Mitochondria have long been known to play a critical role in maintaining the bioenergetic status of cells under physiological conditions. Mitochondria produce large amounts of free radicals, and mitochondrial oxidative damage can contribute to a range of degenerative conditions including cardiovascular diseases (CVDs). Although the molecular mechanisms responsible for mitochondrion-mediated disease processes are not correctly understood, oxidative stress seems to play an important role. Consequently, the selective inhibition of mitochondrial oxidative damage is an obvious therapeutic strategy. This review considers the process of CVD from a mitochondrial perspective and provides a summary of the following areas: reactive oxygen species (ROS) production and its role in pathophysiological processes such as CVD, currently available antioxidants and possible reasons for their efficacy and inefficacy in ameliorating oxidative stress-mediated diseases, and recent developments in mitochondria-targeted antioxidants that concentrate on the matrix-facing surface of the inner mitochondrial membrane. These mitochondrion-targeted antioxidants have been developed by conjugating the lipophilic triphenylphosphonium cation to antioxidant moieties such as ubiquinol. These compounds pass easily through biological membranes and, due to their positive charge, they accumulate several-hundred-fold within mitochondria. In this way they protect against mitochondrial oxidative damage and show potential as a future therapy for CVDs.

Topics: Antioxidants; Cardiovascular Diseases; Diabetes Mellitus; Endothelium, Vascular; Humans; Membrane Potentials; Mitochondria; Mitochondrial Diseases; Nitric Oxide; Organophosphorus Compounds; Oxidative Stress; Reactive Oxygen Species; Reperfusion Injury; Risk Factors; Ubiquinone

Coenzyme Q (ubiquinone, 2-methyl-5,6-dimethoxy-1,4-benzoquinone), soluble natural fat quinine, is crucial to optimal biological function. The coenzyme Q molecule has amphipathic (biphasic) properties due to the hydrophilic benzoquinone ring and the lipophilic poly isoprenoid side-chain. The nomenclature of coenzyme Q-n is based on the amount of isoprenoid units attached to 6-position on the benzoquinone ring. It was demonstrated that coenzyme Q, in addition to its role in electron transport and proton transfer in mitochondrial and bacterial respiration, acts in its reduced form (ubiquinol) as an antioxidant. Coenzyme Q-10 functions as a lipid antioxidant regulating membrane fluidity, recycling radical forms of vitamin C and E, and protecting membrane phospholipids against peroxidation. The antioxidant property, high degree of hydrophobicity and universal occurrence in biological system, suggest an important role for ubiquinone and ubiquinol in cellular defense against oxidative damage. Coenzyme Q-10 is a ubiquitous and endogenous lipid-soluble antioxidant found in all organisms. Neurodegenerative disorders, cancer, cardiovascular diseases and diabetes mellitus and especially aging and Alzheimer's disease exhibit altered levels of ubiquinone or ubiquinol, indicating their likely crucial role in the pathogenesis and cellular mechanisms of these ailments. This review is geared to discuss the biological effect of coenzyme Q with an emphasis on its impact in initiation, progression, treatment and prevention of neurodegenerative, cardiovascular and carcinogenic diseases.

Topics: Aging; Animals; Antioxidants; Cardiovascular Diseases; Diabetes Mellitus; Humans; Lipid Peroxidation; Neoplasms; Neurodegenerative Diseases; Oxidative Stress; Ubiquinone

Topics: Coenzymes; Diabetes Mellitus; Humans; Reference Values; Ubiquinone

Diabetes mellitus associated with mitochondrial tRNA mutation at position 3243(DM-Mt3243) is a new disease. Patients have a distinctly different picture from MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes). During observations at the Saiseikai Central Hospital, the following findings were noted in DM-Mt3243 patients: DM-Mt3243 patients are diagnosed earlier with diabetes, compared to NIDDM (non-insulin dependent diabetes mellitus) controls without family history. DM-Mt3243 patients often need insulin more often than NIDDM controls without family history. Post-treatment neuropathy and insulin edema are often found in DM-Mt3243, and the two phenomena possibly have a similar pathophysiology related to mitochondrial dysfunction. Ambiguous psychiatric disorders of functional psychosis are observed frequently in DM-Mt3243. Mild headache is common in DM-Mt3243 cases. Ambiguous neuromuscular abnormalities such as sleep disturbance, paresthesia of the legs, edema of the legs, and palpitation may be symptoms associated with mitochondrial dysfunction in DM-Mt3243. Coenzyme Q may be effective in the relief of these neuromuscular symptoms.

Topics: Adult; Aged; Clinical Trials as Topic; Coenzymes; Depression; Diabetes Mellitus; Diabetes Mellitus, Type 2; Diagnosis, Differential; DNA, Mitochondrial; Edema; Female; Humans; Insulin; Male; Middle Aged; Mitochondrial Encephalomyopathies; Peripheral Nervous System Diseases; Point Mutation; Psychotic Disorders; RNA, Transfer, Leu; Ubiquinone

We hypothesized that the addition of coenzyme Q10 (CoQ10) to pregabalin might be helpful in improving symptoms in patients suffering from painful diabetic neuropathy (PDN).. One hundred twelve patients with PDN were randomly allocated to receive CoQ10 + pregabalin (57 patients) or placebo + pregabalin (55 patients). Besides pregabalin (150 mg/day), the patients, upon their group assignment, received CoQ10 at a dosage of 100 mg every 8 h or matched placebo for 8 consecutive weeks. The primary efficacy measure was the changes in the pain intensity from baseline to endpoint measured on an 11-point NRS (numeric rating scale). Secondary efficacy measures included the changes in the pain-associated sleep interference score (SIS) as well as the patients' global improvement with treatment measured on the Clinicians' and Patients' Global Impression of Change (CGIC/PGIC).. On the intent‑to‑treat population (ITT) analysis, the CoQ10 + pregabalin regimen resulted in significantly greater pain relief than the placebo + pregabalin regimen. By the end of week 2, the decrease in the mean pain NRS score was similar in both groups, but at the end of weeks four and eight, the decrease in the mean pain NRS score was significantly greater in patients taking CoQ10 + pregabalin than in those taking placebo + pregabalin (p value = 0.01 and < 0.001, respectively). Likewise, at the end of week 8, the decrease in the pain-associated SIS was significantly greater in the patients supplemented with CoQ10 compared to placebo. Furthermore, the proportion of the responder patients (those having ≥ 50% decline in the mean pain NRS score) as well as the proportion of patients rated ''very much'' or ''much improved'' on the CGIC/PGIC scales were also significantly higher in the CoQ10 + pregabalin-treated patients than placebo + pregabalin-treated patients.. Our data support the idea that diabetic patients suffering from PDN may benefit from using antioxidant and anti-inflammatory supplements like CoQ10. However, further studies are required before supplementation with CoQ10 can be recommended for treating PDN.. The trial was registered at Iranian Registry of Clinical Trials (identifier code: IRCT20120215009014N385). Registration date: 2021-02-21.

Topics: Analgesics; Diabetes Mellitus; Diabetic Neuropathies; Double-Blind Method; gamma-Aminobutyric Acid; Humans; Iran; Pain; Pregabalin; Treatment Outcome; Ubiquinone

Im Rahmen der vorliegenden Studie sollte der Einfluss des Weichteilschadens auf das klinische Ergebnis nach offener Ellenbogenluxation untersucht werden.. Von Oktober 2008 bis August 2015 wurden insgesamt 230 Patienten mit Ellenbogenluxation behandelt. Diese retrospektive Studie umfasst 21 Fälle von offenen Ellenbogenluxationen. Das Durchschnittsalter der Patienten betrug 49 Jahre alt (20–83 Jahre), 6 Patienten waren weiblich (29%), 15 männlich (71%). Das Bewegungsausmaß des verletzten und unverletzten Ellenbogens wurde erhoben und das funktionelle Ergebnis u. a. mittels Mayo Elbow Performance Score (MEPS), Mayo Wrist Score (MWS) und dem Disability of Arm, Shoulder and Hand (DASH) Score erfasst. Zusätzlich wurden Komplikationen und Revisionsoperationen aufgezeichnet. Der Einfluss des Weichteilschadens (I°/II° offen vs. III° offen) und des Luxationstyps (einfach vs. komplex) auf das klinische Ergebnis wurde analysiert.. Offene Ellenbogenluxationen können mit einem zufriedenstellenden klinischen Ergebnis einhergehen. Insbesondere komplexe offene Ellenbogenluxationen sind jedoch sehr komplikationsbehaftet, wobei neurovaskuläre Komplikationen am häufigsten auftreten.. The current high rate of multidrug-resistant gram-negative bacteria infections among hospitalised patients with cUTIs in the studied area is alarming. Our predictive model could be useful to avoid inappropriate antibiotic treatment and implement antibiotic stewardship policies that enhance the use of carbapenem-sparing regimens in patients at low risk of multidrug-resistance.. The results indicated differential patterns of Inhibition of Return between the High and Low shape/weight based self-worth groups. The High group displayed increased inhibition of return for the shape/weight stimuli relative to control stimuli, while the Low group displayed reduced inhibition of return for the shape/weight stimuli compared to control stimuli. The ED group displayed a similar pattern of results to the High group, but this did not reach significance.. The current findings indicate that young women without an eating disorder who base their self-worth on shape/weight display a pattern of avoidance of shape/weight stimuli that is in direct contrast to those at low risk of developing eating disorders. The possible implications of these specific patterns of inhibition of return across those at varying levels of risk for an eating disorder are discussed along with their implications for intervention approaches.. These results indicated that Sr. An unusually high HbA

Topics: Activities of Daily Living; Acute Disease; Adalimumab; Adaptation, Physiological; Adenosine Triphosphate; Adipose Tissue; Administration, Intravaginal; Adolescent; Adsorption; Adult; Adverse Childhood Experiences; Age Distribution; Age Factors; Aged; Aged, 80 and over; Air Pollution, Indoor; Aldehyde Oxidase; Alginates; Alloys; alpha-Globins; Aluminum Hydroxide; Alveolar Bone Loss; Anaerobiosis; Anesthesia, General; Anesthetics; Animals; Anovulation; Anti-Bacterial Agents; Anti-Infective Agents; Anti-Inflammatory Agents, Non-Steroidal; Antibodies, Monoclonal, Humanized; Antineoplastic Agents; Apoptosis; Bacillus cereus; Bacterial Typing Techniques; Bacteroidetes; Base Composition; Biocompatible Materials; Biofilms; Biological Availability; Biological Transport; Biosensing Techniques; Bipolar Disorder; Blood Glucose; Body Mass Index; Bone Regeneration; Boranes; Brachial Artery; Butyric Acid; Candida albicans; Carbon; Carcinoembryonic Antigen; Cell Differentiation; Cell Line, Tumor; Cell Respiration; Cell Survival; Cells, Cultured; Cerebrovascular Circulation; Charcoal; Child; Child Health; China; Chloride Channels; Chlorides; CHO Cells; Chromatography, Liquid; Chromatography, Micellar Electrokinetic Capillary; Chromium; Chronic Disease; Chronic Periodontitis; Circular Dichroism; Cities; Cohort Studies; Comamonadaceae; Comorbidity; Coronary Artery Disease; Corrosion; Cricetinae; Cricetulus; Cross Infection; Cross-Sectional Studies; Crowding; Culture Media; Cytokines; Diabetes Mellitus; Diabetes Mellitus, Type 2; Diabetes, Gestational; Diarylheptanoids; Diclofenac; Disability Evaluation; Diterpene Alkaloids; DNA; DNA Mutational Analysis; DNA, Bacterial; Drug Liberation; Drug Resistance, Multiple, Bacterial; Electrochemical Techniques; Electrodes; Electrolytes; Endothelium, Vascular; Enterococcus faecalis; Epithelial Cell Adhesion Molecule; Epithelial Cells; Erbium; Erythropoietin; Ethanol; Ethylenediamines; Fast Foods; Fatty Acids; Female; Fermentation; Ferric Compounds; 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Rats; Rats, Wistar; Receptors, Thyrotropin; Recombinant Proteins; Reproducibility of Results; Republic of Korea; Retrospective Studies; Rhodobacteraceae; Risk; Risk Assessment; Risk Factors; RNA, Ribosomal, 16S; ROC Curve; Saccharomyces cerevisiae; Salinity; Saliva; Seawater; Seaweed; Sensitivity and Specificity; Sequence Analysis, DNA; Sex Factors; Silver Compounds; Smokers; Social Class; Socioeconomic Factors; Soil Microbiology; Solubility; Soy Foods; Spectrometry, Mass, Electrospray Ionization; Spondylitis, Ankylosing; Staphylococcus aureus; Static Electricity; Steroids; Strontium; Sucrose; Surface Properties; Survival Rate; Sweden; Swine; Synapses; Synchrotrons; Tandem Mass Spectrometry; Tannins; Tea; Temperature; Terpenes; Thalidomide; Thermodynamics; Thiadiazoles; Thyroid Cancer, Papillary; Thyroid Neoplasms; Thyroidectomy; Time Factors; Tissue Distribution; Titanium; Toilet Facilities; Tomography, Emission-Computed, Single-Photon; Treatment Outcome; Ubiquinone; Urinary Tract Infections; Vaginal Creams, Foams, and Jellies; Venezuela; Vitamin K 2; Waist Circumference; Waste Disposal, Fluid; Wastewater; Water Microbiology; Water Pollutants, Chemical; Whole Body Imaging; X-Ray Diffraction; Young Adult; Ytterbium; Yttrium; Yttrium Radioisotopes; Zinc Compounds

Selenium and coenzyme Q10 are important antioxidants in the body. As the intake of selenium is low in Europe, and the endogenous production of coenzyme Q10 decreases as age increases, an intervention trial using selenium and coenzyme Q10 for four years was performed. As previously reported, the intervention was accompanied by reduced cardiovascular mortality. The objective of the present study was to analyze cardiovascular mortality for up to 10 years after intervention, to evaluate if mortality differed in subgroups differentiated by gender, diabetes, ischemic heart disease (IHD), and functional class.. Four-hundred forty-three healthy elderly individuals were included from a rural municipality in Sweden. All cardiovascular mortality was registered, and no participant was lost to the follow-up. Based on death certificates and autopsy results mortality was registered.. Significantly reduced cardiovascular mortality could be seen in those on selenium and coenzyme Q10 intervention. A multivariate Cox regression analysis demonstrated a reduced cardiovascular mortality risk in the active treatment group (HR: 0.51; 95%CI 0.36-0.74; P = 0.0003). The reduced mortality could be seen to persist during the 10-year period. Subgroup analysis showed positive effects in both genders. An equally positive risk reduction could be seen in those with ischemic heart disease (HR: 0.51; 95%CI 0.27-0.97; P = 0.04), but also in the different functional classes.. In a 10-year follow-up of a group of healthy elderly participants given four years of intervention with selenium and coenzyme Q10, significantly reduced cardiovascular mortality was observed. The protective action was not confined to the intervention period, but persisted during the follow-up period. The mechanism explaining the persistency remains to be elucidated. Since this was a small study, the observations should be regarded as hypothesis-generating.

Topics: Aged; Aged, 80 and over; Antioxidants; Cardiovascular Diseases; Diabetes Mellitus; Dietary Supplements; Double-Blind Method; Female; Follow-Up Studies; Humans; Male; Myocardial Ischemia; Prospective Studies; Selenium; Sex Distribution; Ubiquinone

The characteristic clinical features of diabetes mellitus with mitochondrial DNA (mtDNA) 3243(A-G) mutation are progressive insulin secretory defect, neurosensory deafness and maternal inheritance, referred to as maternally inherited diabetes mellitus and deafness (MIDD). A treatment for MIDD to improve insulin secretory defects and reduce deafness has not been established. The effects of coenzyme Q10 (CoQ10) treatment on insulin secretory response, hearing capacity and clinical symptoms of MIDD were investigated. 28 MIDD patients (CoQ10-DM), 7 mutant subjects with impaired glucose tolerance (IGT), and 15 mutant subjects with normal glucose tolerance (NGT) were treated daily with oral administration of 150 mg of CoQ10 for 3 years. Insulin secretory response, blood lactate after exercise, hearing capacity and other laboratory examinations were investigated every year. In the same way we evaluated 16 MIDD patients (control-DM), 5 mutant IGT and 5 mutant NGT subjects in yearly examinations. The insulin secretory response assessed by glucagon-induced C-peptide secretion and 24 h urinary C-peptide excretion after 3 years in the CoQ10-DM group was significantly higher than that in the control-DM group. CoQ10 therapy prevented progressive hearing loss and improved blood lactate after exercise in the MIDD patients. CoQ10 treatment did not affect the diabetic complications or other clinical symptoms of MIDD patients. CoQ10 treatment did not affect the insulin secretory capacity of the mutant IGT and NGT subjects. There were no side effects during therapy. This is the first report demonstrating the therapeutic usefulness of CoQ10 on MIDD.

Topics: Adult; C-Peptide; Coenzymes; Deafness; Diabetes Complications; Diabetes Mellitus; Diabetic Nephropathies; Diabetic Neuropathies; Diabetic Retinopathy; DNA, Mitochondrial; Family Health; Female; Glucagon; Glucose Intolerance; Glucose Tolerance Test; Hearing; Humans; Lactic Acid; Male; Middle Aged; Mothers; Point Mutation; Time Factors; Treatment Outcome; Ubiquinone

Reactive oxygen species (ROS) are overproduced in diabetic wounds and retard the healing response. Considering the antioxidative function of idebenone, its exogenous administration may quench excessive ROS and promote diabetic wound healing. In the current study, idebenone was loaded into polyvinyl alcohol (PVA) /calcium alginate scaffolds at three different concentrations of 1 w/w%, 2 w/w%, and 3 w/w%. Various in vitro experiments were performed to characterize the developed wound dressings. Cell viability assay showed that scaffolds loaded with 1 w/w% idebenone had significantly better protection under oxidative stress and exhibited higher cell viability. Therefore, the dressings containing 1% drug was chosen to treat diabetic wounds in rat model. Wound healing assay showed that the dressings loaded with 1% drug had significantly higher rate of wound size reduction, collagen deposition, and epithelial thickness. Gene expression study showed that wound healing was accompanied by modulation of inflammatory response, protection against oxidative stress, and increasing angiogenesis-related genes. This preliminary research suggests that PVA/calcium alginate/1% idebenone scaffolds can be considered as a potential treatment modality to treat diabetic wounds in the clinic. However, more extensive studies at gene and protein expression levels are required to understand its exact mechanism of healing effects.

Topics: Alginates; Animals; Bandages; Diabetes Mellitus; Down-Regulation; Fibroblast Growth Factor 2; Interleukin-1beta; Polyvinyl Alcohol; Rats; Reactive Oxygen Species; Rodent Diseases; Ubiquinone; Up-Regulation; Wound Healing

Diabetes mellitus (DM) is associated with impaired hippocampal synaptic plasticity. Coenzyme Q10 (CoQ10) acts as an antioxidant and exerts neuroprotective effects. Accordingly, this study aimed at evaluating the effects of CoQ10 on hippocampal long-term potentiation (LTP) and paired-pulse facilitation (PPF) in streptozotocin (STZ)-induced diabetic rats. Male Wistar rats were randomly divided into six groups (n = 8 per group) as follows and treated for 90 days: the control, control + low dose of CoQ10 (100 mg/kg), control + high dose of CoQ10 (600 mg/kg), diabetic, diabetic + low dose of CoQ10, and diabetic + high dose of CoQ10 groups. Diabetes was induced by a single intraperitoneal injection of 50 mg/kg STZ. The population spike (PS) amplitude and slope of excitatory post synaptic potentials (EPSPs) were measured in dentate gyrus (DG) area in response to the stimulation applied to the perforant path (PP). The results showed that the STZ-induced diabetes impaired LTP induction in the PP-DG synapses. This finding is supported by the decreased EPSP slope and PS amplitude of LTP (P < 0.05). Both low- and high-dose CoQ10 supplementation in the control and diabetic animals enhanced EPSP slope and PS amplitude of LTP in the granular cells of DG (P < 0.05). PPF was affected by LTP induction in diabetic animals receiving the high dose of CoQ10 (P < 0.05). It is suggested that CoQ10 administration could attenuate deteriorative effect of STZ-induced diabetes on in vivo LTP in the DG. The enhanced transmitter release can be partly one of the possible underlying mechanism(s) responsible for the LTP induction in the diabetic animals treated with CoQ10.

Topics: Animals; Antioxidants; Dentate Gyrus; Diabetes Mellitus; Diabetes Mellitus, Experimental; Long-Term Potentiation; Male; Neurons; Neuroprotective Agents; Rats, Wistar; Streptozocin; Ubiquinone

Coenzyme Q10 (CoQ10) has antioxidant effects and is commercially available and marketed extensively. However, due to its low bioavailability, its effects are still controversial. We developed a water-soluble CoQ10-based micelle formulation (CoQ10-W) and tested it in an experimental model of tacrolimus (TAC)-induced diabetes mellitus (DM).. We developed CoQ10-W from a glycyrrhizic-carnitine mixed layer CoQ10 micelle preparation based on acyltransferases. TAC-induced DM rats were treated with either lipid-soluble CoQ10 (CoQ10-L) or CoQ10-W for 4 weeks. Their plasma and pancreatic CoQ10 concentrations were measured using liquid chromatography- tandem mass spectrometry. The therapeutic efficacies of CoQ10-W and CoQ10-L on TAC-induced DM were compared using functional and morphological parameters and their effects on cell viability and reactive oxygen species (ROS) production were also evaluated in cultured rat insulinoma cells.. The plasma CoQ10 level was significantly increased in the CoQ10-W group compared to that in the CoQ10-L group. Intraperitoneal glucose tolerance tests and glucose-stimulated insulin secretion revealed that CoQ10-W controlled hyperglycemia and restored insulin secretion significantly better than CoQ10-L. The TAC-mediated decrease in pancreatic islet size was significantly attenuated by CoQ10-W but not by CoQ10-L. TAC-induced oxidative stress and apoptosis were significantly more reduced by CoQ10-W than CoQ10-L. Electron microscopy revealed that CoQ10-W restored TAC-induced attenuation in the number of insulin granules and the average mitochondrial area, unlike CoQ10-L. In vitro studies showed that CoQ10-L and CoQ10-W both improved cell viability and reduced ROS production in TAC-treated islet cells to a similar extent.. CoQ10-W has better therapeutic efficacy than CoQ10-L in TAC-induced DM.

Topics: Animals; Diabetes Mellitus; Models, Theoretical; Rats; Tacrolimus; Ubiquinone; Water

COQ2 mutations cause a rare infantile multisystemic disease with heterogeneous clinical features. Promising results have been reported in response to Coenzyme Q10 treatment, especially for kidney involvement, but little is known about the long-term outcomes.. We report four new patients from two families with the c.437G→A (p.Ser146Asn) mutation in COQ2 and the outcomes of two patients after long-term coenzyme Q10 treatment.. Index cases from two families presented with vomiting, nephrotic range proteinuria, and diabetes in early infancy. These patients were diagnosed with coenzyme Q10 deficiency and died shortly after diagnosis. Siblings of the index cases later presented with neonatal diabetes and proteinuria and were diagnosed at the first day of life. Coenzyme Q10 treatment was started immediately. The siblings responded dramatically to coenzyme Q10 treatment with normalized glucose and proteinuria levels, but they developed refractory focal clonic seizures beginning at three months of life that progressed to encephalopathy.. In our cohort with CoQ10 deficiency, neurological involvement did not improve with oral coenzyme Q10 treatment despite the initial recovery from the diabetes and nephrotic syndrome.

Topics: Adaptor Proteins, Vesicular Transport; Ataxia; Cohort Studies; Diabetes Mellitus; Family Health; Female; Humans; Infant; Kidney; Magnetic Resonance Imaging; Male; Mitochondrial Diseases; Muscle Weakness; Mutation; Proteinuria; Ubiquinone

Topics: Diabetes Mellitus; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Risk Factors; Ubiquinone

Statins significantly reduce cardiovascular events in a broad population of patients with hyperlipidemia. However, a small, but significant risk of new-onset diabetes has been reported in patients treated with statins. The mechanism by which statins cause diabetes has not been elucidated and therefore preventive strategies have yet to be defined.. Our goal was to study the differing effects of a lipophilic (simvastatin) statin, hydrophilic (pravastatin) statin, and ezetimibe on glucose transporter-4 (GLUT4) protein expression in 3T3-L1 adipocytes. We hypothesized that the reductions in GLUT4 protein secondary to statin treatment would be prevented when cells were co-incubated with coenzyme Q10 (CoQ10). GLUT4 protein expression was determined using the In-Cell Western technique. Confluent adipocytes were differentiated using a hormonal cocktail for 3 days; followed by treatment with simvastatin, pravastatin, ezetimibe and CoQ10. Cell morphology was observed after treatment using phase-contrast microscopy.. Treatment with simvastatin (P<0.001) and simvastatin plus ezetimibe (P<0.001) significantly decreased GLUT4 protein expression in the adipocytes compared to control conditions. GLUT4 protein levels were similar to control after treatment with ezetimibe alone (P=0.52) or pravastatin (P=0.32). There was no significant difference (P=0.098) in GLUT4 protein levels after co-treatment with CoQ10 between any of the treatments and control conditions.. Our studies have shown that lipophilic statins (simvastatin) reduce the GLUT4 protein levels in adipocytes, whereas hydrophilic statins (pravastatin) or ezetimibe do not. Co-treatment with CoQ10 appears to prevent the reduction in GLUT4 protein levels caused by simvastatin.

Topics: 3T3-L1 Cells; Adipocytes; Animals; Anticholesteremic Agents; Azetidines; Diabetes Mellitus; Drug Interactions; Ezetimibe; Glucose Transporter Type 4; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Insulin Resistance; Mice; Pravastatin; Simvastatin; Ubiquinone

Complementary and alternative medicine (CAM) is common in patients with chronic disease such as diabetes mellitus. The primary objective of the study was to determine the overall prevalence and type of CAM use in individuals with diabetes mellitus (DM) in Western Sydney and to compare the prevalence and factors associated with CAM use with the literature.. A multicenter cross-sectional study was undertaken using a self-completed questionnaire distributed to patients with DM attending a public hospital and specialist endocrinology clinics in the region. The type of DM and pattern of CAM utilisation were analyzed.. Sixty nine people responded to the questionnaire: age range of 18-75 years during a twelve week collection period. Overall, 32 respondents with diabetes were using some form of CAM, resulting in a utilisation rate of 46.3%. Twenty of the 32 CAM users used CAM specifically to treat their diabetes accounting for 28.9% of the respondent sample population. Multivitamins (40%), cinnamon, Co-enzyme q10 and prayer were the most frequently used CAM modalities. There was no significant difference between males and females, age range, income or diabetes complications between CAM and non-CAM users. (p values each > 0.05) The factor most significantly associated with CAM usage was being born overseas (p = 0.044).. Almost half the respondents (46.3%) used CAM: 28% used CAM specifically to treat their diabetes. Individuals born overseas were significantly more likely to use CAM than those born in Australia. Other factors such as age, gender, wealth and duration of living with diabetes were not associated with higher rate of CAM usage.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Australia; Cinnamomum zeylanicum; Complementary Therapies; Cross-Sectional Studies; Diabetes Mellitus; Dietary Supplements; Faith Healing; Female; Health Care Surveys; Humans; Male; Middle Aged; Patient Acceptance of Health Care; Phytotherapy; Plant Extracts; Religion; Residence Characteristics; Surveys and Questionnaires; Ubiquinone; Vitamins; Young Adult

Maternally inherited diabetes and deafness (MIDD) has been related to an A to G transition in the mitochondrial tRNA Leu (UUR) gene at the base pair 3243. This subtype of diabetes is characterized by maternal transmission, young age at onset and bilateral hearing impairment. Besides diabetes and deafness, the main diagnostic features, a wide range of multisystemic symptoms may be associated with the A3243G mutation. Organs that are most metabolically active, such as muscles, myocardium, retina, cochlea, kidney and brain are frequently affected. Gastrointestinal tract symptoms are also common in patients with mitochondrial disease and constipation and diarrhea are the most frequent manifestations. However, there are few prior reports of intestinal pseudo obstruction in MIDD patients. Here we report the case of a patient with MIDD associated with the mtDNA A3243G mutation who developed chronic intestinal pseudo obstruction, and the introduction of Coenzyme Q10 as adjunctive therapy led to a solution of the pseudo obstruction.

Topics: Deafness; Diabetes Complications; Diabetes Mellitus; DNA, Mitochondrial; Female; Humans; Intestinal Pseudo-Obstruction; Middle Aged; Pedigree; Point Mutation; Ubiquinone; Vitamins

To assess the beta-cell function in individuals with mitochondrial DNA A3243G mutation with normal glucose tolerance (NGT) or diabetes mellitus (DM). Furthermore, in diabetic individuals, we evaluated the effect of coenzyme Q10 supplementation on insulin secretory response.. Eight mutation-positive individuals with NGT (n = 4) or DM (n = 4) were studied. beta-Cell function was evaluated by C-peptide levels before and after a mixed liquid meal (Sustacal) challenge and by first-phase insulin response.. Fasting and Sustacal-stimulated C-peptide levels were significantly lower in diabetic patients than that in controls (area under the curve: 104.1 +/- 75.7 vs 520.8 +/- 173.8, P = 0.001), whereas in individuals with NGT, this response was preserved (area under the curve: 537.8 +/- 74.3 vs 520.8 +/- 179.8, P = 0.87). The duration of diabetes was negatively correlated with fasting C-peptide levels (r = -0.961, P = 0.038). Among the 3 patients with residual insulin secretion, the short-term treatment with coenzyme Q10 (3 months) improved C-peptide levels in 2 of them. The first-phase insulin response was diminished in 2 individuals with NGT, the oldest ones.. We showed an impaired insulin secretory capacity in individuals carrying the A3243G mutation, this possibly being the primary defect contributing to the development of DM. In addition, our data suggest that this could be a functional defect.

Topics: Adult; C-Peptide; Coenzymes; Diabetes Mellitus; DNA, Mitochondrial; Female; Glucose Intolerance; Glucose Tolerance Test; Humans; Insulin; Insulin-Secreting Cells; Male; Pedigree; Point Mutation; RNA, Transfer, Leu; Ubiquinone; Vitamins

Oxidative stress is defined as an imbalance between the production of reactive oxygen species (ROS) and the antioxidant network, in favour of the former. Our lifestyle (smoking, alcoholism, obesity, intense physical exercise), but also our inadequate diet, contributes to significantly increase the production of ROS in our organism. This is potentially associated with an increased risk of developing ageing-related pathologies such as cardiovascular diseases and cancer. As a matter of prevention, it is necessary to have in hands a high technology allowing to correctly evidence the oxidative stress status of an individual in order to render optimal our antioxidant defences and to decrease the oxidative damages in DNA, proteins and lipids.

Topics: Amino Acids; Antioxidants; Ascorbic Acid; Biomarkers; Carotenoids; Coenzymes; Diabetes Mellitus; DNA Damage; Electron Transport Chain Complex Proteins; Free Radicals; Glutathione Peroxidase; Glycation End Products, Advanced; Humans; Lipoproteins; Membrane Lipids; Oxidative Stress; Reactive Oxygen Species; Superoxide Dismutase; Superoxides; Thioredoxins; Trace Elements; Ubiquinone; Vitamin E; Vitamins

Several studies have been carried out to evaluate the alterations in mitochondrial functions of diabetic rats. However, results are sometimes controversial, since experimental conditions diverge, including age and strain of used animals. The purpose of this study was to evaluate the metabolic modifications in liver mitochondria, both in the presence of severe (STZ-treated rats) and mild hyperglycaemia [Goto-Kakizaki (GK) rats], when compared with control animals of similar age. Moreover, metabolic alterations were evaluated also at initial and advanced stages of the disease. We observed that both models of diabetes (type 1 and type 2) presented a decreased susceptibility of liver mitochondria to the induction of permeability transition (MPT). Apparently, there is a positive correlation between the severity of diabetes mellitus (and duration of the disease) and the decline in the susceptibility to MPT induction. We also found that liver mitochondria isolated from diabetic rats presented some metabolic adaptations, such as an increase in coenzyme Q and cardiolipin contents, that can be responsible for the observed decrease in the susceptibility to multiprotein pore (MPTP) opening.

Topics: Animals; Calcium; Cardiolipins; Diabetes Mellitus; Liver; Mitochondria; Rats; Ubiquinone

Topics: Adenosine Triphosphate; Anticholesteremic Agents; Biological Transport; Cholesterol; Clinical Trials as Topic; Coenzymes; Diabetes Mellitus; Glucose; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Lovastatin; Protein Prenylation; Terpenes; Ubiquinone

We report the case of 71-year-old male who was once diagnosed as having diabetic amyotrophy, because of pronounced wasting in proximal muscles, massive weight loss, and development of paresthesia in his legs. Afterwards, ragged red fibers and mitochondrial tRNA mutation at position 3243 were documented in muscle biopsy. He had diabetes mellitus associated with 3243 mitochondrial DNA mutation, suggesting that clinically, diabetic amyotrophy may be overlapped with mitochondria-related disease entities in some parts. Coenzyme Q10 administration was effective in relieving the symptoms in his legs, fatigue, and residual urine in his bladder. These were confirmed with the improvement in neurological parameters. In conclusion, this case gives important help in understanding myopathy in diabetes. It would be important to check on the 3243 mitochondrial tRNA mutation in patients with diabetic amyotrophy and/or diabetic neuropathic symptoms.

Topics: Animals; Coenzymes; Diabetes Complications; Diabetes Mellitus; Humans; Male; Muscular Diseases; Mutation; RNA; RNA, Mitochondrial; RNA, Transfer, Leu; Ubiquinone

Topics: Adult; Diabetes Mellitus; Female; Humans; Mitochondria; Point Mutation; RNA, Transfer, Leu; Ubiquinone

Available evidence--some well-documented, some only preliminary--suggests that properly-designed nutritional insurance supplementation may have particular value in diabetes. Comprehensive micronutrient supplementation providing ample doses of antioxidants, yeast-chromium, magnesium, zinc, pyridoxine, gamma-linolenic acid, and carnitine, may aid glucose tolerance, stimulate immune defenses, and promote wound healing, while reducing the risk and severity of some of the secondary complications of diabetes.

Topics: Animals; Antioxidants; Ascorbic Acid; Calcium; Carnitine; Chromium; Diabetes Mellitus; gamma-Linolenic Acid; Humans; Linolenic Acids; Magnesium; Pyridoxine; Selenium; Thioctic Acid; Ubiquinone; Vitamin E; Zinc

"Eumetabolic" therapies of diabetes are defined as those which promote and potentiate a normal physiological pattern of insulin activity--in contrast to the less subtle effects of exogenous insulin or sulfonylureas. Effective eumetabolic therapy would provide better metabolic control and reduce the risk of secondary complications, would be more convenient to administer, and would be especially appropriate for preventive use in the early stages of diabetes. Possible components of a eumetabolic therapy include: aspirin, as a potentiator of glucose-stimulated insulin secretion; GTF, to directly enhance the efficacy of insulin; weight loss, exercise, and fasting, to help reduce tissue resistance to insulin; mitochondrial "metavitamins", to optimize the oxidative disposal of excess substrate; a high-fiber, low-fat diet, which appears superior to traditional diabetic diets as a promoter of glucose tolerance. Following a prolonged fast, obese diabetics show substantial improvement in most parameters of insulin function--an effect which is to some degree independent of weight loss; long-term remission of diabetes may be possible if the benefits of therapeutic fasting are conserved by appropriate eumetabolic measures.

Topics: Amino Acids; Aspirin; Carnitine; Chromium; Diabetes Mellitus; Dietary Fats; Dietary Fiber; Fasting; Humans; Nicotinic Acids; Organometallic Compounds; Pyridoxine; Thioctic Acid; Ubiquinone

The activity of the succinate dehydrogenase-coenzyme Q10 reductase from 120 diabetic patients was significantly lower (P less than 0.001) and the per cent deficiency was significantly higher (P less than 0.001) than that of the controls. The diabetes of 37 patients was controlled by diet; the enzyme activity was lower (P less than 0.001) and the deficiency was higher (P less than 0.02) than for controls. In decreasing effectiveness, Dymelor, Glyburide, Phenformin and Tolazamide inhibited the COQ10-enzyme, NADH-oxidase. Tolbutamide, Glypizide, and Chlorpropamide were noninhibitory to succinoxidase and NADH-oxidase. Patients receiving Tolazamide and Phenformin showed a higher incidence (P less than 0.001 to P less than 0.05) of COQ10-deficiency than patients controlled by diet or normal controls. Certain diabetic patients controlled by diet may have a deficiency of COQ10 which may be enhanced by the inhibition by certain commonly used antidiabetic drugs of COQ10-enzymes. A deficiency of COQ10 in the pancreas could impair bioenergetics, the generation of ATP, and the biosynthesis of insulin.

Topics: Adult; Aged; Diabetes Mellitus; Female; Humans; Hypoglycemic Agents; Leukocytes; Male; Middle Aged; NADH, NADPH Oxidoreductases; Succinate Dehydrogenase; Ubiquinone

Topics: Animals; Blood Glucose; Cytochromes; Diabetes Mellitus; Male; Mitochondria, Liver; Oxidation-Reduction; Pancreatectomy; Rats; Ubiquinone

Topics: Acetates; Animals; Cytoplasm; Diabetes Mellitus; Glycerol; Injections, Intramuscular; Lactates; Liver; Malates; Male; NAD; Oxaloacetates; Oxidation-Reduction; Phosphates; Pyruvates; Rats; Ubiquinone

Topics: Coenzymes; Diabetes Mellitus; Quinones; Ubiquinone