Additional Supplements That Support Glycemic Control and Reduce Chronic Inflammation
Robert Fried, Richard M. Carlton in Type 2 Diabetes, 2018
Coenzyme Q10 (CoQ10) is also known as ubiquinone. A coenzyme is a non-protein compound that is required for the biological activity of a protein. CoQ10 is ubiquitous in animals and in most bacteria, hence the name ubiquinone. This fat-soluble substance, which resembles a vitamin, is present in all respiring eukaryotic cells, primarily in the mitochondria. It participates in the cellular aerobic respiration, which generates energy in the form of ATP. It is estimated that 95% of the human body energy is generated this way. Therefore, those organs with the highest energy requirements—such as the heart, liver, and kidney—also have the highest CoQ10 concentrations (Okamoto, Matsuya, Fukunaga et al. 1989; Aberg, Appelkvist, Dallner et al. 1992). There are three redox states of CoQ10: (1) fully oxidized (ubiquinone), (2) semiquinone (ubisemiquinone), and (3) fully reduced (ubiquinol). The capacity of this molecule to act as a two-electron carrier, moving between the quinone and quinol form, and a one-electron carrier, moving between the semiquinone and one of these other forms, is central to its role in the electron transport chain due to the iron–sulfur clusters that can only accept one electron at a time and as a free-radical–scavenging antioxidant. The journal Clinical Biochemist Reviews published a detailed report on CoQ10, titled “Coenzyme Q10: is there a clinical role and a case for measurement?” (Molyneux, Young, Florkowski et al. 2008). Some of the critical issues it detailed are described below. CoQ10 deficiency has been implicated in several clinical disorders, including hypertension and heart failure.
ENZYME-CATALYZED REACTIONS
David M. Gibson, Robert A. Harris in Metabolic Regulation in Mammals, 2001
Glucose in its capacity as fuel is oxidized to lactate ("anaerobic" glycolysis, Chapter5) or to CO, and water ("aerobic" glycolysis plus citric acid cycle, Chapter6) through a succession of coupled cnzymc-catalvzcd steps. While the llux of organic intermediates can Ih- followed sequentially from glucose to lactate or to CO, the intervention of complex resident cellular molecules, the coenzymes, is observed at many steps which couple glycolysis to side reactions and to other metabolic pathways. m many enzyme-cataly/ed reactions, coenzymes are me 'second substrate", the concentration ot which can severely limit the rates of conversion■ 2.2.1 COENZYME PAIRSThe designation coenzyme is historical in that these molecules were discovered as complcx organic cofactors which were necessary lor the expressed activity ol certain enzvmcs. lor example, the coenzyme NAD' (nicotinamide adenine dinuclcotidc) was required for the enzyme alcohol dehydrogenase to catalyze the conversion of ethanol to acetaldehyde. In this reaction two protons and two electrons were conveyed Iront the ethanol substrate to NAD* forming NADU and a free proton (H+). Coenzymes, like enzymes, exist in relatively minute concentrations in the cell and promote the llux of organic intermediates through both the oxidative and synthetic pathways. Coenzymes in fact are co-substrates for various enzymes by accepting or delivering chemical groups from or to the principal organic substrates (or even by transferring the activated substrate itself). Thus each coenzyme exists in at least two forms: the first with and the second without the transferred entity. The total concentration of a coenzyme pair in a cellular domain is usually constant. A consequence of the fixed, low concentrations of coenzymes in the cell is that they must shuttle rapidiv between two or more states, i.e. turn over. Ilcing tied up in one form or the other, i.e. unable to turn over, can bring metabolic flux to a halt, figure 2.1 illustrates several coenzymes. 'Essential' organic nutrients, such as wtamins and certain fatty acids and amino acids, cannot be synthesized in arwnal cells■ 2.2.2 VITAMINSMany coenzymes are synthesized Iron» vitamin precursors. For example, the vitamin nicotinic add (or nicotinamide) is incorporated into the structures of NAD* and NADP+. A vitamin is an essential part of the animal diet since enzymes catalyzing its formation have In-en lost from the genome, or the rate of synthesis of the vitamin is not commensurate w ith cell growth and maintenance. If these precursors are not supplied a spectrum of deficiency diseases may develop.
Oxidative Stress and the Effects of Dietary Supplements on Glycemic Control in Type 2 Diabetes
Emmanuel C. Opara, Sam Dagogo-Jack in Nutrition and Diabetes, 2019
Blood glucose regulation is dependent upon normal glucose metabolism, which, in turn, is regulated by chains of reactions catalyzed by enzymes. Some enzymes require no chemical groups other than their amino residues for activity, and others require an additional chemical component referred to as a cofactor. The cofactor may be either one or more inorganic ions or a complex organic or metallorganic molecule called a coenzyme. Certain enzymes require both a coenzyme and one or more metal ions for activity. These metal ions are usually transition metals, which are obtained from the diet in small (micrograms and milligrams) amounts, hence the term trace elements. As already mentioned, some of these elements are present in the cells and tissues as cofactors of certain antioxidant enzymes, such as zinc in superoxide dismutase (SOD) and selenium in glutathione peroxidase (GPx). As transition metals, the trace elements have antioxidant potential, and the effect of supplementation with certain trace elements on glycemic control has been examined in diabetic patients.
An Improvement of Oxidative Stress in Diabetic Rats by Ubiquinone-10 and Ubiquinol-10 and Bioavailability after Short- and Long-Term Coenzyme Q
Published in Journal of Dietary Supplements, 2016
Pattaneeya Prangthip, Aikkarach Kettawan, Juthathip Posuwan, Masaaki Okuno, Tadashi Okamoto
This study explored effects of ubiquinol-10 and ubiquinone-10, two different forms of coenzyme Q10, in diabetic rats. Oxidative stress is characterized by the depletion of antioxidant defenses and overproduction of free radicals that might contribute to, and even accelerate, the development of diabetes mellitus (DM) complications. Coenzyme Q10 was administered orally to diabetic rats and oxidative stress markers were then assessed. Bioavailability in normal rats was additionally assessed in various tissues and subcellular fractions after short-term and long-term coenzyme Q10 supplementation. Elevated nonfasting blood glucose and blood pressure in diabetic rats were decreased by ubiquinone-10. Both ubiquinol-10 and ubiquinone-10 ameliorated oxidative stress, based on assays for reactive oxygen metabolites and malondialdehyde. Coenzyme Q10 levels increased with both treatments and liver nicotinamide adenine dinucleotide phosphate (NADPH) coenzyme Q reductase with ubiquinone-10. Ubiquinol-10 was better absorbed in the liver and pancreas than ubiquinone-10, though both were similarly effective. In bioavailability study, a longer period of coenzyme Q10 supplementation did not lead to its accumulation in tissues or organelles. Both forms of coenzyme Q10 reduced oxidative stress in diabetic rats. Long-term supplementation of coenzyme Q10 appeared to be safe.
Improved photostability and cytotoxic effect of coenzyme Q10 by its association with vitamin E acetate in polymeric nanocapsules
Published in Pharmaceutical Development and Technology, 2018
Natháli S. Pegoraro, Juliane Mattiazzi, Elita F. da Silveira, Juliana H. Azambuja, Elizandra Braganhol, Letícia Cruz
The present study showed the development of nanocapsules containing the association of the coenzyme Q10 and vitamin E acetate and the evaluation of their effect on in vitro cells culture of malignant glioma and melanoma. In order to investigate if nanocapsules are able to protect coenzyme Q10 from degradation under UVC radiation, a photostability study was carried out. For this, three concentrations of vitamin E acetate were evaluated (1%, 2%, or 3%). Nanocapsules presented suitable physicochemical characteristics and were able to protect coenzyme Q10 from photodegradation. In addition, this protection was influenced by higher vitamin E acetate concentrations, attributing to this oil an important role on coenzyme Q10 photostabilization. Regarding to in vitro citotoxicity assay, nanocapsules containing coenzyme Q10 and 2% vitamin E significantly reduced glioma and melanoma cell viability in 61% and 66%, respectively. In this sense, these formulations represent interesting platforms for the delivery of coenzyme Q10 and vitamin E acetate, presenting effect on the reduction of malignant cells viability.
Serum paraoxonase 1 status and its association with atherogenic indexes in gentamicin-induced nephrotoxicity in rats treated with coenzyme Q10
Published in Renal Failure, 2014
Hassan Ahmadvand, Maryam Ghasemi Dehnoo, Akram Dehghani, Shahrokh Bagheri, Rooh Angiz Cheraghi
Coenzyme Q10 is a natural antioxidant and scavenger of free radicals. In the present study, we examined the effect of coenzyme Q10 on paraoxonase 1 (PON1) activity, lipid profile, atherogenic indexes and relationship of PON 1 activity by high-density lipoprotein (HDL) and atherogenic indexes in gentamicin (GM)-induced nephrotoxicity rats. Thirty Sprague–Dawley rats were divided into three groups to receive saline; GM, 100 mg/kg/d; and GM plus coenzyme Q10 by 15 mg/kg i.p daily, respectively. After 12 days, animals were anaesthetized, blood samples were also collected before killing to measure the levels of triglyceride (TG), cholesterol (C), low-density lipoprotein (LDL), very low density lipoprotein (VLDL), HDL, atherogenic indexes and the activities of PON1 of all groups were analyzed. Data were analyzed by non-parametric Mann–Whitney test (using SPSS 13 software). Coenzyme Q10 significantly decreased TG, C, LDL, VLDL, atherogenic index, atherogenic coefficient and cardiac risk ratio. HDL level and PON1 activity were significantly increased when treated with coenzyme Q10. Also, the activity of PON 1 correlated positively with HDL and negatively with atherogenic coefficient, cardiac risk ratio 1 and cardiac risk ratio 2. This study showed that coenzyme Q10 exerts beneficial effects on PON1 activity, lipid profile, atherogenic index and correlation of PON 1 activity with HDL and atherogenic index in GM -induced nephrotoxicity rats.
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