Effects of coenzyme Q10 on health-related quality of life, clinical disease activity and blood pressure in patients with mild to moderate ulcerative colitis: a randomized clinical trial

Farsi, Farnaz; Ebrahimi‐Daryani, Nasser; Barati, Mahmood; Janani, Leila; Karimi, Mahdi; Akbari, Abolfazl; Irandoost, Pardis; Alamdari, Naimeh Mesri; Agah, Shahram; Vafa, Mohammadreza

doi:10.47176/mjiri.35.3

Cited by 7 publications

(7 citation statements)

References 46 publications

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“…CoQ10 supplementation in UC patients, also decreased the severity of inflammation and reduced blood pressure (72). As ubiquinone-2 was increased in the intestine, liver, and spleen, it can be suggested that increasing biosynthesis or supplementation would not only reduce inflammation in the intestine but could have a systemic protective effect, increasing its usefulness as a therapeutic target (71)(72)(73). The molecule putatively identified as epoxydocosapentaenoic acid (EDP) was increased in the ileum, colon, and spleen of colitis mice.…”

Section: Discussionmentioning

confidence: 85%

“…During LPS induced stress, ubiquinol treatment blocks protein kinase C (PKC) activity and improves mitochondrial function, preventing ROS generation and cellular damage (71). CoQ10 supplementation in UC patients, also decreased the severity of inflammation and reduced blood pressure (72). As ubiquinone-2 was increased in the intestine, liver, and spleen, it can be suggested that increasing biosynthesis or supplementation would not only reduce inflammation in the intestine but could have a systemic protective effect, increasing its usefulness as a therapeutic target (71)(72)(73).…”

Section: Discussionmentioning

confidence: 99%

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Spatial mapping of dextran sodium sulphate-induced intestinal inflammation and its systemic effects

Adams,

Rasid,

Hulme

et al. 2024

Preprint

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Inflammatory bowel disease (IBD) is a multifactorial disease and patients frequently experience extraintestinal manifestations affecting multiple sites. Causes of systemic inflammation remain poorly understood but molecules originating from the intestine likely play a role with microbial and host small molecules polarizing host immune cells towards a pro- or anti-inflammatory phenotype. Using the dextran sodium sulphate (DSS) mouse model, which mimics models the disrupted barrier function in IBD, microbial dysbiosis and immune cell dysregulation in IBD, we investigated metabolomic and phenotypic changes at intestinal and systemic sites. Through mass spectrometry imaging we mapped the spatial distribution and relative abundance of molecules and cell types across a range of tissues during colitis. This approach revealed specific molecular changes across a range of organs including the colon, ileum, liver, spleen and kidney, while no molecular changes were observed in the lungs of DSS-treated mice. Specific molecules, identified as contributing to the statistical separation of treated from control mice, were then spatially localized within organs to determine their effects on cellular phenotypes through imaging mass cytometry. Additionally, molecules that were significantly changed across multiple systemic sites in response to inflammation were identified. This spatial approach identified drivers of inflammation both locally in the intestine and systemically and has highlighted a number of molecules not previously implicated in inflammation linked to IBD or the systemic effects of intestinal inflammation. Together this data shows that gaining a better understanding of metabolic pathways and identifying molecular disease biomarkers within the intestine and systemic organs during IBD, might improve our understanding of disease aetiology and aid the development of new targeted therapies.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Spatial mapping of dextran sodium sulphate-induced intestinal inflammation and its systemic effects

Adams,

Rasid,

Hulme

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

“…In a randomised controlled clinical trial, supplementation with CoQ10 (200 mg/day for 8 weeks) significantly reduced levels of inflammatory markers and disease severity, and improved quality of life in patients with mild to moderate ulcerative colitis [62,63]. There are no studies listed on Medline relating to CoQ10 and Crohn's disease, celiac disease, irritable bowel syndrome or gastric reflux.…”

Section: Gastrointestinal Disordersmentioning

confidence: 99%

Depletion and Supplementation of Coenzyme Q10 in Secondary Deficiency Disorders

Mantle¹,

Turton²,

Hargreaves³

2022

Front. Biosci. (Landmark Ed)

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Coenzyme Q10 (CoQ10) deficiency is broadly divided into two types, primary and secondary. Primary CoQ10 deficiencies are relatively rare disorders resulting from mutations in genes directly involved in the CoQ10 biosynthetic pathway, and are not a subject of this article. Secondary CoQ10 disorders are relatively common, and may occur for a variety of reasons; these include mutations in genes not directly related to the synthetic pathway, oxidative stress induced reduction of CoQ10, and the effects of pharmacological agents such as statins. CoQ10 is of key importance in cell metabolism; in addition to its role in mitochondrial oxidative phosphorylation, it is a major endogenous antioxidant, and has a role in the metabolism of sulphides, lipids and amino acids. Given its importance in cell metabolism, it is unsurprising that secondary CoQ10 deficiency has been linked with a wide range of disorders. In this article, we have reviewed evidence of secondary CoQ10 deficiency in both common and less common disorders, and highlighted those disorders in which CoQ10 supplementation has been shown to be of significant clinical benefit.

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“…Ubiquinone has shown to alleviate disease expression in animal models, [49][50][51][52][53][54] reduce apoptosis through mitochondrial mechanisms, 55,56 and in the context of clinical trials for UC, decrease disease expression and increase patient quality of life. 57 Although studies assessing the production of ubiquinone by R. sphaeroides in an intestinal environment are lacking, it was found that administration of R. sphaeroides in bovine significantly increased the ubiquinone content of the milk by over 70%, 58 thus suggesting that production in a mammalian intestinal environment is not only possible but of significant yield.…”

Section: Rhodobacter Sphaeroidesmentioning

confidence: 99%

The Case for Rhodobacter Sphaeroides as a probiotic: Applications for Human Health and Ulcerative Colitis

St-Laurent

2022

UOJM

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In this short review, the mechanisms through which the probiotic administration of non-pathogenic bacterium Rhodobacter Sphaeroides could contribute to human health in general, and more specifically, the treatment of ulcerative colitis, are explored. This review is built around the concept that the mitochondrion is the key player in the pathogenesis of ulcerative colitis, and proposes ways that the probiotic could contribute to a more optimal environment for mitochondrial functioning, namely through reduction of inflammation and production of beneficial compounds like ubiquinone and bacteria-derived carotenoids. It concludes with the current state of the research involving Rhodobacter Sphaeroides as a probiotic and suggests possible future directions.

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Effects of coenzyme Q10 on health-related quality of life, clinical disease activity and blood pressure in patients with mild to moderate ulcerative colitis: a randomized clinical trial

Cited by 7 publications

References 46 publications

Spatial mapping of dextran sodium sulphate-induced intestinal inflammation and its systemic effects

Spatial mapping of dextran sodium sulphate-induced intestinal inflammation and its systemic effects

Depletion and Supplementation of Coenzyme Q10 in Secondary Deficiency Disorders

The Case for Rhodobacter Sphaeroides as a probiotic: Applications for Human Health and Ulcerative Colitis

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