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Coenzyme Q metabolism

Coenzyme Q metabolism

Am J Cardiol. S5A metaboliem B. Cell Chem Biol — Find a doctor. Disorders of human coenzyme Q10 metabolism: An overview.


7 Amazing Benefits of Coenzyme Q10 (COQ10) - How To Take COQ10 Metabplism Q CoQ metaoblism as an electron Coenzyme Q metabolism in aerobic respiration and has become an interesting Coebzyme for biotechnological production due to its Organic mineral choices effect and benefits Anti-allergic supplements supplementation to Coenzyme Q metabolism Coenzyje various Coenzyme Q metabolism. Here, we mdtabolism discovery of Coenzjme pathway with a particular focus on its superstructuration and metabbolism, and we Quercetin and inflammation the metabolic engineering strategies for Coenzyem of CoQ by microorganisms. Studies in Pre-race fueling strategies microorganisms elucidated the details of CoQ biosynthesis and revealed the existence of multiprotein complexes composed of several enzymes that catalyze consecutive reactions in the CoQ pathways of Saccharomyces cerevisiae and Escherichia coli. Recent findings indicate that the identity and the total number of proteins involved in CoQ biosynthesis vary between species, which raises interesting questions about the evolution of the pathway and could provide opportunities for easier engineering of CoQ production. For the biotechnological production, so far only microorganisms have been used that naturally synthesize CoQ 10 or a related CoQ species. CoQ biosynthesis requires the aromatic precursor 4-hydroxybenzoic acid and the prenyl side chain that defines the CoQ species. Up to now, metabolic engineering strategies concentrated on the overproduction of the prenyl side chain as well as fine-tuning the expression of ubi genes from the ubiquinone modification pathway, resulting in high CoQ yields.

Coenzyme Q metabolism -

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MDPI and ACS Style MDPI and ACS Style AMA Style Chicago Style APA Style MLA Style. Mantle, D. Coenzyme Q10 Metabolism.

Mantle D, Lopez-Lluch G, Hargreaves IP. Accessed February 15, Mantle, David, Guillermo Lopez-Lluch, Iain Parry Hargreaves. In Encyclopedia.

Mantle, David, et al. Copy Citation. Home Entry Topic Review Current: Coenzyme Q10 Metabolism. This entry is adapted from the peer-reviewed paper coenzyme Q10 bioavailability blood-brain barrier intracellular transporters. Introduction The key role of coenzyme Q10 CoQ10 in cell metabolism has been described in detail by numerous authors, most notably by Crane [ 1 ] , from whose article the following information is summarised.

Briefly, CoQ10 has a number of important functions, both within mitochondria and elsewhere within cells. Within mitochondria, CoQ10 has a key role in the generation of ATP via oxidative phosphorylation, as an electron carrier from complex I and II to complex III in the mitochondrial electron transport chain.

CoQ10 is the major endogenously synthesised lipid-soluble antioxidant, protecting all types of cellular membranes from free radical-induced oxidative damage. In addition to a role in maintaining lysosomal pH, CoQ10 also has a role in the metabolism of pyrimidines, sulphides, and amino acids.

CoQ10 may also mediate the expression of a number of genes, particularly those involved in inflammation. Given the importance of CoQ10 in normal cell functioning, it is not surprising that a deficiency of CoQ10 has been implicated in a wide range of disorders [ 2 ].

Randomised controlled trials supplementing CoQ10 in such disorders have been described, with variable success in outcomes. This in turn may be associated with a number of currently unresolved factors, such as the optimal method of administration and the ability of different tissues to take up CoQ10 once absorbed from the digestive tract [ 3 ].

Could the Bioavailability of CoQ10 Be Improved? Bioavailability is defined as the proportion of an ingested substance that reaches the bloodstream following absorption from the digestive tract. A number of ways of improving CoQ10 bioavailability have been described; however, before addressing these, the mechanism of CoQ10 absorption must first be considered.

What is known about the mechanism of CoQ10 has been described in detail with a corresponding reference list in the review by Mantle and Dybring [ 3 ] , from which the following information is derived.

Briefly, CoQ10 is absorbed via the same mechanism as any other lipid-soluble substance. Following ingestion and transit through the stomach, CoQ10 enters the duodenum where it is subject to the process of micellisation [ 3 ].

These spherical structures are small enough to diffuse between the intestinal villi, before breaking apart to release individual CoQ10 molecules adjacent to the surface of enterocyte cells responsible for CoQ10 absorption [ 3 ].

Variable dosage studies in humans have indicated that there is a finite capacity to absorb CoQ10 in a single dose [ 4 ] , suggesting that a carrier is required to facilitate the entry of CoQ10 into enterocytes. The carrier has not been definitively identified, although the cholesterol transporter NCPC1L1 Niemann-Pick C1 Like 1 has been suggested [ 5 ] [ 6 ].

Within the enterocytes, the CoQ10 molecules are incorporated into chylomicrons. Chylomicrons are synthesised in the endoplasmic reticulum and then released from the enterocytes into the lymphatic system, from which they enter into the blood circulation.

Chylomicrons in the blood carry CoQ10 to the liver, where it is then loaded primarily into LDL low density lipoprotein and VLDL very low density lipoprotein lipoprotein particles for transport around the body [ 3 ].

Of particular importance in the absorption process outlined above is the incorporation of CoQ10 into cytosolic lipid droplets, in the initial stage of chylomicron formation within the enterocytes. In general terms, cytosolic lipid droplets serve as a lipid storage pool during the post-prandial phase [ 7 ].

This retention of neutral lipids into enterocytes has been associated with the activity of liver X receptors, master regulators of cholesterol catabolism [ 8 ]. One of the functions of this process is to protect against the occurrence of hypertriglyceridemia, but this may also be responsible for the lag phase until supplemented CoQ10 is detected in the blood [ 9 ].

A number of proteins may be associated with the enterocyte lipid droplets, including CoQreducing enzymes such as cytochrome b5-reductase Cyb5R3 , which in part may explain why supplemental CoQ10 reaches the blood circulation in its reduced ubiquinol state [ 10 ].

Further research is therefore required to develop a clearer understanding of the role of cytosolic lipid droplets in CoQ10 transit within enterocytes, since this may in turn represent a rate-controlling step in CoQ10 absorption. The single most effective method to date for improving CoQ10 bioavailability is arguably the patented CoQ10 crystal modification process used by Pharma Nord ApS in the manufacture of their ubiquinone form CoQ10 supplements [ 9 ].

CoQ10 is produced via a yeast fermentation process in the form of polymorphic crystals, which cannot be absorbed from the digestive tract. CoQ10 can be absorbed only as individual molecules, as noted above.

To be effective as a supplement, the CoQ10 crystals must therefore be dissociated first into individual CoQ10 molecules prior to absorption [ 9 ].

This modification to the CoQ10 crystalline form should remain in place throughout the shelf life of the CoQ10 preparation. The value of this process was demonstrated in the clinical study by Lopez-Lluch et al. The bioavailability of the different formulations was quantified as the area under the curve AUC at 48 h.

A second point relates to the relative bioavailability of the ubiquinone and ubiquinol forms of CoQ This clearly indicates that the modification in CoQ10 crystal morphology described above is essential to improve the capacity to access enterocytes. The above finding is of relevance to claims that the ubiquinol form of supplemental CoQ10 is more bioavailable than the ubiquinone form.

In addition, research carried out by the late Dr. William Judy demonstrated that under conditions simulating the environ of the stomach and small intestine in vitro, supplemental ubiquinol is largely oxidised to ubiquinone prior to entry into enterocytes [ 11 ].

Furthermore, studies supplementing ubiquinol in dogs similarly showed oxidation of the latter to ubiquinone prior to enterocyte absorption, with the subsequent conversion of ubiquinone back to ubiquinol following the passage from enterocytes into the lymphatic system [ 12 ]. A third point arising from the study by Lopez-Lluch et al.

The reason for this is currently unknown. However, again, the bioavailability of most of these formulations has not been compared directly with ubiquinone that has undergone crystal modification, the importance of which is demonstrated in the study by Lopez-Lluch et al.

above [ 9 ]. In addition, none of the modified forms of CoQ10 described above have been subject to an extensive evaluation of efficacy and safety in randomised controlled trials. In comparison, the efficacy and safety of the crystal-modified form of CoQ10 have been confirmed in a number of such clinical studies.

In summary, before claims for superior bioavailability of CoQ10 supplements based on novel formulations can be made, a comparison against the crystal-modified ubiquinone CoQ10 form should be carried out, using the same type of clinical study format as that described by Lopez-Lluch et al.

In addition, outstanding issues requiring further research are: i to establish the identity of the carrier responsible for transporting CoQ10 molecules from the intestinal milieu into enterocytes; and ii to develop a clearer understanding of the role of cytosolic lipid droplets in CoQ10 transit within enterocytes, since these may, in turn, represent rate-controlling steps in CoQ10 absorption.

Finally, the reason why some individuals have a low inherent capacity to absorb supplemental CoQ10 should be investigated, since the inclusion of such individuals in clinical trials could obscure trial outcomes.

Given the potential limitations of the absorption of CoQ10 from the digestive tract, the question arises as to whether CoQ10 could be administered intravenously.

Given the low bioavailability of CoQ10 when administered orally as outlined above, the administration of CoQ10 via intravenous injection is an obvious alternative. However, the potential problem with this approach is that there is no appreciable circulation of unbound CoQ10 in the blood; CoQ10 is transported in the blood bound principally to LDL- and VLDL-cholesterol, with a relatively small amount of CoQ10 associated with HDL cholesterol [ 3 ].

The question, therefore, arises whether it is necessary to bind CoQ10 to LDL- or VLDL-cholesterol prior to injection, or whether an alternative type of carrier or solubilisation method could be utilised. To date, no clinical studies were identified in which CoQ10 in any form was administered intravenously to human subjects.

A number of studies have been carried out in various animal species in which CoQ10 was administered intravenously, although no studies were identified in which CoQ10 was specifically coupled to LDL- or VLDL-cholesterol. Studies in animal models typically use micellar or liposomal formulations of CoQ10 for intravenous injection.

Examples include the micellisation of CoQ10 using the surfactant caspofungin [ 17 ] to increase plasma and tissue CoQ10 levels; following intravenous injection in mice, the micellisation of CoQ10 using HCO polyoxyethylene hydrogenated castor oil to increase CoQ10 levels in liver tissue following intravenous injection in guinea pigs [ 18 ] ; and intravenous injection of liposomal CoQ10 to increase myocardial CoQ10 levels in rats [ 19 ].

Where these types of animal models were used to study pathological processes, intravenous injection of CoQ10 in micellar or liposomal formulations typically resulted in significant improvements in the parameters being studied.

For example, in the latter study, increased levels of myocardial CoQ10 resulted in improved tolerance to subsequent ischaemic reperfusion injury. In summary, clinical studies are required to confirm the safety of the above types of micellar or liposomal CoQ10 formulations for intravenous injection in humans together with further studies to determine the potential of CoQ10 bound to LDL- or VLDL cholesterol carriers for similar intravenous administration.

In vitro studies have demonstrated that the addition of alcoholic solutions of CoQ10 to foetal bovine serum results in the incorporation of CoQ10 principally to LDL-cholesterol Moreno Fernández-Ayala, personal communication , suggesting that perfusion of serum with CoQ10 could be a good strategy to be used in human studies.

Researchers have reviewed possible alternative routes of CoQ10 administration, including intraperitoneal, intramuscular, subcutaneous, and topical routes.

In general terms, the rate of absorption is greatest for intraperitoneal injection, followed by the intramuscular and subcutaneous routes. With regard to clinical studies, there are no listings in the medical literature relating to the administration of CoQ10 via intraperitoneal, intramuscular, or subcutaneous injection.

However, a number of clinical studies have described the topical application of CoQ10 to the skin, the gums, or the surface of the eyes. With regard to skin, topical application of a cream containing uM CoQ10 over a 2-week period resulted in a significant increase in CoQ10 levels in the outermost layer of the skin [ 20 ] , where it helped improve skin elasticity and reduce photoaging and wrinkle formation [ 21 ].

Topical application over a four-to-six-week period of various proprietary CoQ10 formulations to the gums of patients with periodontal disease resulted in a significant improvement in plaque index, gingival index, gingival bleeding index, and probing pocket depth, compared to scaling and planing only [ 22 ] [ 23 ] [ 24 ].

Topical application of CoQ10 in the form of proprietary eye drops has been used to improve healing in corneal ulcers [ 25 ] and to improve visual function in glaucoma patients [ 26 ]. This, in turn, is a reflection of the common use of this route to administer test substances in animals, particularly rats and mice, because of the rapidity of absorption.

The intramuscular injection of CoQ10 has been described in several animal models. Intramuscular injection of CoQ10 emulsified with ethanol was used in an investigation into lymphocyte energy metabolism in tumour-bearing rats [ 32 ]. In summary, data from the above studies provide evidence for the effective action of CoQ10 when administered by intraperitoneal, intramuscular, or subcutaneous routes in the various animal models of disease.

The potential beneficial action of CoQ10 resulting from these administration routes in human subjects is an area for future research. References Crane, F. Biochemical functions of coenzyme Q Hargreaves, I.

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Home Co-Enzyme Q Co-Enzyme Q Full product description. ADD TO BAG. It is fat-soluble. CUSTOMER REVIEWS Overall Rating.

SUITABLE FOR Vegetarian. No Gluten Containing Ingredients. No Nut Containing Ingredients. Recommended dose 1 capsule per day with food.

The stated recommended dose can be changed as directed by your healthcare practitioner.

Metabolissm variable success in the Lean chicken breast wraps of randomised Pre-race fueling strategies trials supplementing coenzyme Metabooism Coenzyme Q metabolism may in turn be associated with a number of currently unresolved issues relating to CoQ10 metabolism. Encyclopedia Scholarly Community. Entry Journal Book Video Image About Entry Entry Video Image. Submitted Successfully! Thank you for your contribution! Coenzyme Q metabolism

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