The effect of ubiquinone in diabetic polyneuropathy: A randomized double-blind placebo-controlled study

Hernández-Ojeda, Jaime; Cardona-Muñoz, Ernesto Germán; Román-Pintos, Luis Miguel; Troyo-Sanromán, Rogelio; Ortiz‐Lazareno, Pablo César; Cárdenas-Meza, Mario; Pascoe-González, Sara; Miranda-Díaz, Alejandra Guillermina

doi:10.1016/j.jdiacomp.2012.04.004

Cited by 43 publications

(32 citation statements)

References 26 publications

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“…Clinical observation of endogenous CoQ10 has shown that, in type 2 DM patients, plasma and platelet MDA, as a marker of oxidative stress, were significantly higher, and the level of CoQ10, as antioxidant capacity, was significantly lower compared to controls, with a negative correlation between plasma CoQ10 and HbA1c [146]. When patients with type 2 DM and DPN were supplemented with 400 mg/day of CoQ10, NSS, Neuropathic Disability Score (NDS), and NCS were improved compared to placebo and associated with a reduction in LPO after 12 weeks of treatment [147]. Furthermore, an increase on total antioxidant capacity, anti-inflammatory effects, shown by reduction of CRP, and probably a protective effect on insulin resistance have been proven when supplementing with 200 mg/day of CoQ10 for 12 weeks, although, at this doses, no beneficial effects on clinical and nerve conduction were observed [148].…”

Section: Diabetic Polyneuropathymentioning

confidence: 99%

Diabetic Polyneuropathy in Type 2 Diabetes Mellitus: Inflammation, Oxidative Stress, and Mitochondrial Function

Román-Pintos

Villegas-Rivera

Rodríguez-Carrizález

et al. 2016

Journal of Diabetes Research

181

152

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Diabetic polyneuropathy (DPN) is defined as peripheral nerve dysfunction. There are three main alterations involved in the pathologic changes of DPN: inflammation, oxidative stress, and mitochondrial dysfunction. Inflammation induces activation of nuclear factor kappa B, activator protein 1, and mitogen-activated protein kinases. Oxidative stress induced by hyperglycemia is mediated by several identified pathways: polyol, hexosamine, protein kinase C, advanced glycosylation end-products, and glycolysis. In addition, mitochondrial dysfunction accounts for most of the production of reactive oxygen and nitrosative species. These free radicals cause lipid peroxidation, protein modification, and nucleic acid damage, to finally induce axonal degeneration and segmental demyelination. The prevalence of DPN ranges from 2.4% to 78.8% worldwide, depending on the diagnostic method and the population assessed (hospital-based or outpatients). Risk factors include age, male gender, duration of diabetes, uncontrolled glycaemia, height, overweight and obesity, and insulin treatment. Several diagnostic methods have been developed, and composite scores combined with nerve conduction studies are the most reliable to identify early DPN. Treatment should be directed to improve etiologic factors besides reducing symptoms; several approaches have been evaluated to reduce neuropathic impairments and improve nerve conduction, such as oral antidiabetics, statins, and antioxidants (alpha-lipoic acid, ubiquinone, and flavonoids).

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Section: Diabetic Polyneuropathymentioning

confidence: 99%

Diabetic Polyneuropathy in Type 2 Diabetes Mellitus: Inflammation, Oxidative Stress, and Mitochondrial Function

Román-Pintos

Villegas-Rivera

Rodríguez-Carrizález

et al. 2016

Journal of Diabetes Research

181

152

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“…CoQ10 treatment improves endothelial function and blood flow; thus, long-term treatment may be effective by improving oxygenation of the peripheral nerves (89). Finally, Hernandez-Ojeda et al (90) reported that a 12-wk treatment with ubiquinone significantly improves diabetic polyneuropathy in patients with type 2 diabetes.…”

Section: Activation Of Plcβ3 Causes An Increase In Intracellular Camentioning

confidence: 99%

Coenzyme Q10 prevents peripheral neuropathy and attenuates neuron loss in the db ⁻ /db ⁻ mouse, a type 2 diabetes model

Shi

Zhang

Zeberg³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Diabetic peripheral neuropathy (DPN) is the most common complication in both type 1 and type 2 diabetes. Here we studied some phenotypic features of a well-established animal model of type 2 diabetes, the leptin receptor-deficient db − /db − mouse, and also the effect of long-term (6 mo) treatment with coenzyme Q10 (CoQ10), an endogenous antioxidant. Diabetic mice at 8 mo of age exhibited loss of sensation, hypoalgesia (an increase in mechanical threshold), and decreases in mechanical hyperalgesia, cold allodynia, and sciatic nerve conduction velocity. All these changes were virtually completely absent after the 6-mo, daily CoQ10 treatment in db − /db − mice when started at 7 wk of age. There was a 33% neuronal loss in the lumbar 5 dorsal root ganglia (DRGs) of the db − /db − mouse versus controls at 8 mo of age, which was significantly attenuated by CoQ10. There was no difference in neuron number in 5/6-wk-old mice between diabetic and control mice. We observed a strong down-regulation of phospholipase C (PLC) β3 in the DRGs of diabetic mice at 8 mo of age, a key molecule in pain signaling, and this effect was also blocked by the 6-mo CoQ10 treatment. Many of the phenotypic, neurochemical regulations encountered in lumbar DRGs in standard models of peripheral nerve injury were not observed in diabetic mice at 8 mo of age. These results suggest that reactive oxygen species and reduced PLCβ3 expression may contribute to the sensory deficits in the late-stage diabetic db − /db − mouse, and that early long-term administration of the antioxidant CoQ10 may represent a promising therapeutic strategy for type 2 diabetes neuropathy.is a debilitating complication of both type 1 and type 2 diabetes, affecting up to 50% of diabetes patients (1-5). DPN can be observed early in human diabetes (6, 7). Early neurophysiological studies indicated that at initial stages of the illness, the severity of the polyneuropathy was similar in type 1 and type 2 diabetes patients (8). However, more recent studies showed distinct differences both in humans and rodent models. Thus, progressive axonal atrophy and loss are more serious in type 1 diabetes, which in contrast to type 2 shows nodal and paranodal degenerative changes, as well as more severe downstream effects on neuroskeletal and adhesive proteins (9).In type 1 and type 2 diabetes, many patients initially experience painful diabetic neuropathy, allodynia, which subsides and then is replaced by loss of sensation, hypoalgesia (5, 10, 11). A similar course of disease has been noted in the db /db− mouse, just one of many animal models of diabetes (SI Text), has since then been extensively studied as a particularly robust model for type 2 DPN (14).Previous studies of mammalian DPN models have reported a decrease in impulse conduction velocity (CV) in several peripheral nerves, interpreted as being caused by a reduction in number of large or medium-sized axons (15-20), demyelination (18,19,(21)(22)(23), or axon shrinkage/atrophy (24, 25). Unmyelinated and myelinated fibers in the skin a...

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“…CoQ10 (1) intake in combination with fenofibrate markedly improved both endothelial and non-endothelial vasodilation. CoQ10 (1) improved nerve conduction parameters of diabetic polyneuropathy and reduced oxidative stress without any adverse effects [27]. CoQ10 (1) improved beta cell function and increased insulin sensitivity which reduced insulin requirements for diabetic patients [28].…”

Section: Diabetesmentioning

confidence: 99%

Co-enzyme Q10 (Ubiquinone): It's Implication in Improving the Life Style of the Elderly

Motohashi¹,

Gallagher²,

Venugopalan³

et al. 2018

Med Clin Rev

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Coenzyme Q10 (CoQ10) (1) is lipid-soluble and an important mitochondrial redox component, endogenously produced antioxidant in the human organisms. CoQ10 (1) plays an important role in the production of cellular energy, strengthens the immune system and acts as a free radical scavenger. Aging, poor eating habits, infections and stress affect the amounts of CoQ10 (1) in the humans. As human beings age, they begin to lose the ability to synthesize CoQ10 (1) from food resulting in its deficiency. CoQ10 (1) facilitates the production of adenosine triphosphate (ATP) in the mitochondria by participating in redox reactions within the electron transport chain. Cardiovascular disease deaths in elders are 80% in males and 75% in females. The average age of death from cardiovascular diseases in the developing world is 68 years and in developed world it is 80 years. Cardiovascular disease onset is 7-10 years earlier in men as compared to women. A low level of myocardial CoQ10 (1) is related to the severity of heart failure. Long-term CoQ10 (1) treatment of patients with chronic heart failure is safe and reduces major adverse cardiovascular complications.

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The effect of ubiquinone in diabetic polyneuropathy: A randomized double-blind placebo-controlled study

Cited by 43 publications

References 26 publications

Diabetic Polyneuropathy in Type 2 Diabetes Mellitus: Inflammation, Oxidative Stress, and Mitochondrial Function

Diabetic Polyneuropathy in Type 2 Diabetes Mellitus: Inflammation, Oxidative Stress, and Mitochondrial Function

Coenzyme Q10 prevents peripheral neuropathy and attenuates neuron loss in the db ⁻ /db ⁻ mouse, a type 2 diabetes model

Co-enzyme Q10 (Ubiquinone): It's Implication in Improving the Life Style of the Elderly

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The effect of ubiquinone in diabetic polyneuropathy: A randomized double-blind placebo-controlled study

Cited by 43 publications

References 26 publications

Diabetic Polyneuropathy in Type 2 Diabetes Mellitus: Inflammation, Oxidative Stress, and Mitochondrial Function

Diabetic Polyneuropathy in Type 2 Diabetes Mellitus: Inflammation, Oxidative Stress, and Mitochondrial Function

Coenzyme Q10 prevents peripheral neuropathy and attenuates neuron loss in the db − /db − mouse, a type 2 diabetes model

Co-enzyme Q10 (Ubiquinone): It's Implication in Improving the Life Style of the Elderly

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About

Coenzyme Q10 prevents peripheral neuropathy and attenuates neuron loss in the db ⁻ /db ⁻ mouse, a type 2 diabetes model