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 5 publications

(5 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

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show abstract

“…(39,40) The primary comparison of interest is between the combined intervention versus control. Assuming a mean change in the IBDQ-32 score of 16 ± 20 estimated from previous literature, (41)(42)(43)(44) αsignificance of 0⋅05 and power 95 %, a sample size of n 19 per arm is required with effect size of 0⋅8. To allow for ∼25 % drop-out, given the duration of this trial and based on previous literature, (45)(46)(47) n 25 participants will be recruited to each arm.…”

Section: Recruitmentmentioning

confidence: 99%

The INHABIT (synergIstic effect of aNtHocyAnin and proBIoTics in) Inflammatory Bowel Disease trial: a study protocol for a double-blind, randomised, controlled, multi-arm trial

Cosier,

Lambert,

Batterham

et al. 2024

J Nutr Sci

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Ulcerative Colitis (UC), a type of Inflammatory Bowel Disease (IBD), is a chronic, relapsing gastrointestinal condition with increasing global prevalence. The gut microbiome profile of people living with UC differs from healthy controls and this may play a role in the pathogenesis and clinical management of UC. Probiotics have been shown to induce remission in UC; however, their impact on the gut microbiome and inflammation is less clear. Anthocyanins, a flavonoid subclass, have shown anti-inflammatory and microbiota-modulating properties; however, this evidence is largely preclinical. To explore the combined effect and clinical significance of anthocyanins and a multi-strain probiotic, a 3-month randomised controlled trial will be conducted in 100 adults with UC. Participants will be randomly assigned to one of four groups: anthocyanins (blackcurrant powder) + placebo probiotic, probiotic + placebo fruit powder, anthocyanin + probiotic, or double placebo. The primary outcome is a clinically significant change in the health-related quality-of-life measured with the Inflammatory Bowel Disease Questionnaire-32. Secondary outcomes include shotgun metagenomic sequencing of the faecal microbiota, faecal calprotectin, symptom severity, and mood and cognitive tests. This research will identify the role of adjuvant anti-inflammatory dietary treatments in adults with UC and elucidate the relationship between the gut microbiome and inflammatory biomarkers in this disease, to help identify targeted individualised microbial therapies. ANZCTR registration ACTRN12623000630617.

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“…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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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 5 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

The INHABIT (synergIstic effect of aNtHocyAnin and proBIoTics in) Inflammatory Bowel Disease trial: a study protocol for a double-blind, randomised, controlled, multi-arm trial

Depletion and Supplementation of Coenzyme Q10 in Secondary Deficiency Disorders

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