ubiquinone and Weight-Loss

Oxidative stress is a key player of the inflammatory cascade responsible for the initiation of ulcerative colitis (UC). Although the short chain quinone idebenone is considered a potent antioxidant and a mitochondrial electron donor, emerging evidence suggests that idebenone also displays anti-inflammatory activity. This study evaluated the impact of idebenone in the widely used dextran sodium sulphate (DSS)-induced mouse model of acute colitis. Acute colitis was induced in C57BL/6J mice via continuous exposure to 2.5% DSS over 7 days. Idebenone was co-administered orally at a dose of 200 mg/kg body weight. Idebenone significantly prevented body weight loss and improved the disease activity index (DAI), colon length, and histopathological score. Consistent with its reported antioxidant function, idebenone significantly reduced the colonic levels of malondialdehyde (MDA) and nitric oxide (NO), and increased the expression of the redox factor NAD(P)H (nicotinamide adenine dinucleotide phosphate) dehydrogenase quinone-1 (NQO-1) in DSS-exposed mice. Immunohistochemistry revealed a significantly increased expression of tight junction proteins, which protect and maintain paracellular intestinal permeability. In support of an anti-inflammatory activity, idebenone significantly attenuated the elevated levels of pro-inflammatory cytokines in colon tissue. These results suggest that idebenone could represent a promising therapeutic strategy to interfere with disease pathology in UC by simultaneously inducing antioxidative and anti-inflammatory pathways.

Topics: Administration, Oral; Animals; Anti-Inflammatory Agents; Antioxidants; Colitis; Dextran Sulfate; Disease Models, Animal; Female; Gene Expression Regulation; Humans; Malondialdehyde; Mice; Mice, Inbred C57BL; NAD(P)H Dehydrogenase (Quinone); Nitric Oxide; Ubiquinone; Weight Loss

Body overweight and obesity were considered as a risk factor for many systemic diseases as diabetic hypertension, cardiovascular diseases, and some cancers. The lipoic acid and Co Q are considered as coenzymes needed for enhancement metabolic rate. The goal of this study is to evaluate the anti-obese effect of lipoic acid alone or combined with Co-Q in rats.. Ninety male albino rats (100-150g) were used in this study, divided into six groups (15 each). Group I: Normal rats fed normal diet. Group II: Rats fed high fat diet (HFD). Group III: Rats fed HFD were given lipoic acid (10 μg/kg b w/day) intra-gastric by stomach tube. Group IV: Rats fed HFD were given Co-Q (10 μg/kg b.w/day) intra-gastric. Group V: Rats fed HFD were given lipoic acid (50 mg/kg b w/day) and Co-Q (10 μg/kg b. w/day). Group VI: Rats were given orlistat intra-gastric (10 mg/kg b w/day) as positive control for 6 weeks. Serum was subjected for determination of lipid profile, liver function tests atherogenic factor and lipoprotein lipase.. It was found that treatment with lipoic acid or Co-Q or combined showed increase in the activity of lipoprotein lipase (. lipoic acid combined with Co-Q increase fat oxidation and prevent fat accumulation. The consumption of lipoic acid daily promotes fat oxidation and prevents its accumulation in visceral tissues. Further studies should be carried out to examine the mechanistic signals of these nutrients that helps in weight management.

Topics: Adipogenesis; Animals; Anti-Obesity Agents; Humans; Lipoprotein Lipase; Male; Obesity; Rats; Thioctic Acid; Triglycerides; Ubiquinone; Weight Loss

Oxidative stress is a key factor implicated in the development of diabetic neuropathy. This study evaluates the prophylactic and antinociceptive effects of the antioxidant coenzyme Q10 (CoQ10) on diabetes-induced neuropathic pain in a diabetic mouse model.. Total 56 mice with type 1 diabetes induced by streptozotocin were used, 20 normal mice were used as control. Mechanical and thermal nociceptive behavioral assays were applied to evaluate diabetic neuropathic pain. Tissue lipid peroxidation, immunohistochemistry, reverse transcription, and polymerase chain reaction were used to evaluate the molecular mechanisms of CoQ10. Data are presented as mean ± SEM.. CoQ10 administration was associated with reduced loss of body weight compared with nontreated diabetic mice, without affecting blood glucose levels. Low dose and long-term administration of CoQ10 prevented the development of neuropathic pain. Treatment with CoQ10 produced a significant dose-dependent inhibition of mechanical allodynia and thermal hyperalgesia in diabetic mice. Dorsal root ganglia, sciatic nerve, and spinal cord tissues from diabetic mice demonstrated increased lipid peroxidation that was reduced by CoQ10 treatment. CoQ10 administration was also noted to reduce the proinflammatory factors in the peripheral and central nervous system.. The results of this study support the hypothesis that hyperglycemia induced neuronal oxidative damage and reactive inflammation may be pathogenic in diabetic neuropathic pain. CoQ10 may be protective by inhibiting oxidative stress and reducing inflammation by down-regulating proinflammatory factors. These results suggest that CoQ10 administration may represent a low-risk, high-reward strategy for preventing or treating diabetic neuropathy.

Topics: Analgesics; Animals; Body Weight; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Diabetic Neuropathies; Disease Models, Animal; Dose-Response Relationship, Drug; Lipid Peroxidation; Male; Mice; Mice, Inbred C57BL; Oxidative Stress; Reverse Transcriptase Polymerase Chain Reaction; Ubiquinone; Vitamins; Weight Loss

Genetic endowment and proper training are the major factors contributing to athletic success in endurance and ultraendurance events. Proper nutrition, primarily adequate carbohydrate and fluid, prior to and during the event is also critical. Endurance athletes often utilize other nutritional substances or practices, often referred to as ergogenics, in attempts to obtain a competitive edge by enhancing energy utilization and delaying the onset of fatigue. Numerous nutritional ergogenics have been used in attempts to enhance endurance performance, but with several exceptions most have been shown to be ineffective, including bee pollen, L-carnitine, CoQ10, inosine, amino acids, alkaline salts, and vitamin E at sea level. Research findings are equivocal relative to the ergogenicity of caffeine, phosphate salts, and vitamin E at altitude. Loss of excess body fat, a nutritional practice, may be an effective ergogenic. Conversely, some agents such as alcohol may impair performance, an ergolytic effect. Additional research is necessary to support the efficacy of several nutritional ergogenics to enhance prolonged endurance performance, such as caffeine, phosphates, specific amino acids, and various commercial products. Such research should involve exercise tasks comparable in intensity and duration to that experienced in the marathon and similar endurance events.

Topics: Amino Acids, Branched-Chain; Bicarbonates; Caffeine; Coenzymes; Humans; Nutritional Physiological Phenomena; Phosphorus; Physical Endurance; Sodium; Sodium Bicarbonate; Sports; Task Performance and Analysis; Ubiquinone; Vitamins; Weight Loss