The Role of Methyl Donors of the Methionine Cycle in Gastrointestinal Infection and Inflammation

Vaccaro, Joseph A.; Naser, Saleh A.

doi:10.3390/healthcare10010061

Cited by 11 publications

(6 citation statements)

References 163 publications

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“…The degradation product of trimethylamine that is exclusively produced by gut microbial metabolism. 39 S-Adenosyl-methionine (SAM) 53 A methylation cycle metabolite and methyl donor, 40 SAM-enzymes are key in bacterial host colonization. 41 Hydroxyphenyl pyruvic acid 53 A gut microbial degradation product of the aromatic amino acid tyrosine.…”

Section: Effect Modification By Race Gender and Agementioning

confidence: 99%

Gut microbiota-associated metabolites and risk of ischemic stroke in REGARDS

Ament

Patki

Bhave

et al. 2023

J Cereb Blood Flow Metab

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Several metabolite markers are independently associated with incident ischemic stroke. However, prior studies have not accounted for intercorrelated metabolite networks. We used exploratory factor analysis (EFA) to determine if metabolite factors were associated with incident ischemic stroke. Metabolites (n = 162) were measured in a case-control cohort nested in the REasons for Geographic and Racial Differences in Stroke (REGARDS) study, which included 1,075 ischemic stroke cases and 968 random cohort participants. Cox models were adjusted for age, gender, race, and age-race interaction (base model) and further adjusted for the Framingham stroke risk factors (fully adjusted model). EFA identified fifteen metabolite factors, each representing a well-defined metabolic pathway. Of these, factor 3, a gut microbiome metabolism factor, was associated with an increased risk of stroke in the base (hazard ratio per one-unit standard deviation, HR = 1.23; 95%CI = 1.15–1.31; P = 1.98 × 10−10) and fully adjusted models (HR = 1.13; 95%CI = 1.06–1.21; P = 4.49 × 10−4). The highest tertile had a 45% increased risk relative to the lowest (HR = 1.45; 95%CI = 1.25–1.70; P = 2.24 × 10−6). Factor 3 was also associated with the Southern diet pattern, a dietary pattern previously linked to increased stroke risk in REGARDS (β = 0.11; 95%CI = 0.03–0.18; P = 8.75 × 10−3). These findings highlight the role of diet and gut microbial metabolism in relation to incident ischemic stroke.

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Section: Effect Modification By Race Gender and Agementioning

confidence: 99%

Gut microbiota-associated metabolites and risk of ischemic stroke in REGARDS

Ament

Patki

Bhave

et al. 2023

J Cereb Blood Flow Metab

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“…DNA methyltransferases (DNMTs) transfer the methyl group to cytosine and convert SAM to S-adenosyl homocysteine (SAH) which is further degraded to homocysteine (HCY) by SAH hydrolase ( 16 ). During these processes, vitamin B6 serves as a co-factor ( 17 ). It’s reported that excessive methionine and vitamin B6 intake induces hyper-methylation ( 18 ).…”

Section: Resultsmentioning

confidence: 99%

“…During these processes, vitamin B6 serves as a co-factor (17). It's reported that excessive methionine and vitamin B6 intake induces hypermethylation (18).…”

Section: Melatonin May Play a Key Role In The Genomic Hyper-methylati...mentioning

confidence: 99%

Maternal obesity may disrupt offspring metabolism by inducing oocyte genome hyper-methylation via increased DNMTs

Chao,

Lu,

et al. 2024

Preprint

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Maternal obesity has deleterious effects on oocyte genome methylation establishment, yet the underlying mechanisms remain unclear. In the present study, we first find that maternal obesity induced by high-fat diet (HFD) disturbs genomic methylation in oocytes, and at least a part of the altered methylation is transmitted to F2 oocytes and livers via females. We further identified that altered metabolites such as methionine and melatonin may play a key role in the re-methylation establishment in oocytes of obese mice. Exogenous melatonin treatment significantly reduces the hyper-methylation of HFD oocytes. The higher expression of DNMT3a and DNMT1 in HFD oocytes is also decreased by melatonin supplement, which may be mediated by cAMP/PKA/CREB pathway. These results suggest that maternal obesity-induced genomic methylation alterations in oocytes, can be partly transmitted to F2 in females, and that melatonin is involved in regulating the hyper-methylation of HFD oocytes via increasing the expression of DNMTs mediated by cAMP/PKA/CREB pathway.

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“…Methionine produces strong antioxidative metabolites such as glutathione, cysteine and sulphate through the trans-sulphuration pathway. Previous studies have demonstrated the ameliorative effect of methyl and S-adenosylmethionine produced by the methionine cycle on systemic inflammation and liver damage [ 41 ]. The methionine cycle is widely active in Saccharomyces cerevisiae [ 42 ].…”

Section: Discussionmentioning

confidence: 99%

Anti-Hyperuricemic Effect of Anserine Based on the Gut–Kidney Axis: Integrated Analysis of Metagenomics and Metabolomics

et al. 2023

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Nowadays, developing effective intervention substances for hyperuricemia has become a public health issue. Herein, the therapeutic ability of anserine, a bioactive peptide, was validated through a comprehensive multiomics analysis of a rat model of hyperuricemia. Anserine was observed to improve liver and kidney function and modulate urate-related transporter expressions in the kidneys. Urine metabolomics showed that 15 and 9 metabolites were significantly increased and decreased, respectively, in hyperuricemic rats after the anserine intervention. Key metabolites such as fructose, xylose, methionine, erythronic acid, glucaric acid, pipecolic acid and trans-ferulic acid were associated with ameliorating kidney injury. Additionally, anserine regularly changed the gut microbiota, thereby ameliorating purine metabolism abnormalities and alleviating inflammatory responses. The integrated multiomics analysis indicated that Saccharomyces, Parasutterella excrementihominis and Emergencia timonensis were strongly associated with key differential metabolites. Therefore, we propose that anserine improved hyperuricemia via the gut–kidney axis, highlighting its potential in preventing and treating hyperuricemia.

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The Role of Methyl Donors of the Methionine Cycle in Gastrointestinal Infection and Inflammation

Cited by 11 publications

References 163 publications

Gut microbiota-associated metabolites and risk of ischemic stroke in REGARDS

Gut microbiota-associated metabolites and risk of ischemic stroke in REGARDS

Maternal obesity may disrupt offspring metabolism by inducing oocyte genome hyper-methylation via increased DNMTs

Anti-Hyperuricemic Effect of Anserine Based on the Gut–Kidney Axis: Integrated Analysis of Metagenomics and Metabolomics

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