dietary choline
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Metabolites ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 64
Author(s):  
Bungo Shirouchi ◽  
Ayano Fukuda ◽  
Taiki Akasaka

Choline, betaine, and L-carnitine are transformed into trimethylamine (TMA) by gut microbiota, absorbed into the liver, and oxidized into trimethylamine-N-oxide (TMAO) by flavin-containing monooxygenases. Elevated TMAO levels may negatively affect human health. As phosphatidylcholine (PC) is the main source of dietary choline, its intake or PC-rich foods may be harmful to human health; however, quantitative comparative information among dietary choline compounds (PC, glycerophosphocholine [GPC], and choline chloride [CC]) regarding in vivo generation of TMAO is lacking. Here, we compared the effects of PC, GPC, and CC on plasma TMAO levels in rats. Furthermore, we investigated their effects on gut microbiota at the genus level. Dietary PC did not affect plasma TMAO levels, whereas dietary GPC and CC significantly increased them. At the genus level, plasma TMAO levels were significantly negatively correlated with relative abundances of Anaerotruncus, Actinomyces, Enterococcus, Dialister, Clostridium XIVa, and Granulicatella; they were significantly positively correlated with that of Coprobacter. Moreover, the relative abundances of Anaerotruncus and Coprobacter were found to predict plasma TMAO levels. Therefore, dietary PC, unlike GPC or CC, does not increase plasma TMAO levels in rats. Furthermore, several gut microbes are associated with changes in plasma TMAO levels in rats fed with choline compounds.


2022 ◽  
Vol 21 (1) ◽  
Author(s):  
Mahdieh Golzarand ◽  
Parvin Mirmiran ◽  
Fereidoun Azizi

Abstract Background Several studies have assessed the association between dietary choline and betaine and cardiovascular disease (CVD), but their results are inconsistent. The present study aimed to determine the association between dietary intake of choline and betaine and the risk of CVD in the general population over a 10.6-year period of follow-up. Methods The present cohort study was conducted on participants in the third wave of the Tehran Lipid and Glucose Study (2006–2008) and was followed-up until March 2018. Dietary intake of choline and betaine was calculated using the United States Department of Agriculture (USDA) database. Patients’ medical records were used to collect data on CVD. Results In this study, 2606 subjects with no previous CVD participated and were followed-up for a median of 10.6 years. During the follow-up periods, 187 incidences of CVD were detected. Results of the Cox proportional hazards regression indicated that neither energy-adjusted total choline nor betaine was associated with the incidence of CVD. Among individual choline forms, only higher intake of free choline (FC) was associated with a lower risk of CVD (HR: 0.64, 95% CI: 0.42–0.98). There was no significant association between each 10 mg/d increase in choline and betaine content of each food category and CVD. Conclusion Our investigation indicates no association between energy-adjusted total choline and betaine and a 10.6-year risk of CVD among adults. Besides, we found no relationship between individual choline forms (except FC) and CVD. We also found energy-adjusted choline and betaine obtained from food categories were not associated with the risk of CVD.


2021 ◽  
Vol 15 ◽  
Author(s):  
Sara V. Maurer ◽  
Cuicui Kong ◽  
Niccolò Terrando ◽  
Christina L. Williams

Perioperative neurocognitive disorders (PNDs) are a common complication following procedures such as orthopedic surgery. Using a mouse model of tibial fracture and repair surgery, we have previously shown an increase in neuroinflammation and hippocampal-dependent cognitive deficits. These changes were ameliorated with the addition of a cholinergic agonist. Here, we sought to examine the effects of a high-choline diet for 3 weeks prior to tibial fracture surgery. We evaluated memory using novel object recognition (NOR) as well as young neurons and glial cell morphology at 1 day and 2 weeks post-surgery. At both time points, tibial fracture impaired NOR performance, and dietary choline rescued these impairments. Astrocytic density and hilar granule cells increased 1 day after tibial fracture, and these increases were partially blunted by dietary choline. An increase in young neurons in the subgranular zone of the dentate gyrus was found 2 weeks after tibial fracture. This increase was partially blunted by choline supplementation. This suggests that shortly after tibial fracture, hippocampal reorganization is a possible mechanism for acute impaired memory. These findings together suggest that non-pharmaceutical approaches, such as pre-surgical dietary intervention with choline, may be able to prevent PNDs.


Microbiome ◽  
2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Lesley Hoyles ◽  
Matthew G. Pontifex ◽  
Ildefonso Rodriguez-Ramiro ◽  
M. Areeb Anis-Alavi ◽  
Khadija S. Jelane ◽  
...  

Abstract Background Communication between the gut microbiota and the brain is primarily mediated via soluble microbe-derived metabolites, but the details of this pathway remain poorly defined. Methylamines produced by microbial metabolism of dietary choline and l-carnitine have received attention due to their proposed association with vascular disease, but their effects upon the cerebrovascular circulation have hitherto not been studied. Results Here, we use an integrated in vitro/in vivo approach to show that physiologically relevant concentrations of the dietary methylamine trimethylamine N-oxide (TMAO) enhanced blood-brain barrier (BBB) integrity and protected it from inflammatory insult, acting through the tight junction regulator annexin A1. In contrast, the TMAO precursor trimethylamine (TMA) impaired BBB function and disrupted tight junction integrity. Moreover, we show that long-term exposure to TMAO protects murine cognitive function from inflammatory challenge, acting to limit astrocyte and microglial reactivity in a brain region-specific manner. Conclusion Our findings demonstrate the mechanisms through which microbiome-associated methylamines directly interact with the mammalian BBB, with consequences for cerebrovascular and cognitive function.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yang Li ◽  
Michael Kreuzer ◽  
Quentin Clayssen ◽  
Marc-Olivier Ebert ◽  
Hans-Joachim Ruscheweyh ◽  
...  

AbstractEnteric fermentation from ruminants is a primary source of anthropogenic methane emission. This study aims to add another approach for methane mitigation by manipulation of the rumen microbiome. Effects of choline supplementation on methane formation were quantified in vitro using the Rumen Simulation Technique. Supplementing 200 mM of choline chloride or choline bicarbonate reduced methane emissions by 97–100% after 15 days. Associated with the reduction of methane formation, metabolomics analysis revealed high post-treatment concentrations of ethanol, which likely served as a major hydrogen sink. Metagenome sequencing showed that the methanogen community was almost entirely lost, and choline-utilizing bacteria that can produce either lactate, ethanol or formate as hydrogen sinks were enriched. The taxa most strongly associated with methane mitigation were Megasphaera elsdenii and Denitrobacterium detoxificans, both capable of consuming lactate, which is an intermediate product and hydrogen sink. Accordingly, choline metabolism promoted the capability of bacteria to utilize alternative hydrogen sinks leading to a decline of hydrogen as a substrate for methane formation. However, fermentation of fibre and total organic matter could not be fully maintained with choline supplementation, while amino acid deamination and ethanolamine catabolism produced excessive ammonia, which would reduce feed efficiency and adversely affect live animal performance.


2021 ◽  
Author(s):  
Lisard Iglesias-Carres ◽  
Emily Krueger ◽  
Jacob Herring ◽  
Jeffery Tessem ◽  
Andrew Neilson

Trimethylamine N-oxide (TMAO) is a pro-atherosclerotic product of dietary choline metabolism generated by a microbiome-host axis. The first step in this pathway is enzymatic metabolism of choline to trimethylamine (TMA) by the gut microbiota. This reaction could be targeted to reduce atherosclerosis risk. We aimed to evaluate potential inhibitory effects of select dietary phenolics and their relevant gut microbial metabolites on TMA production via a human ex vivo-in vitro fermentation model. Various phenolics inhibited choline use and TMA production, especially larger compounds or their larger metabolites, without altering cell respiration or cell growth. However, inhibitory effects decreased at late fermentation times, which suggest that these compounds delay choline metabolism rather than completely inhibiting TMA formation. Overall, caffeic acid, catechin and epicatechin were the most effective non-cytotoxic inhibitors of choline use and TMA production. Thus, these compounds are proposed as lead bioactives to test in vivo.


Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2873
Author(s):  
Emily S. Krueger ◽  
Trevor S. Lloyd ◽  
Jeffery S. Tessem

Since elevated serum levels of trimethylamine N-oxide (TMAO) were first associated with increased risk of cardiovascular disease (CVD), TMAO research among chronic diseases has grown exponentially. We now know that serum TMAO accumulation begins with dietary choline metabolism across the microbiome-liver-kidney axis, which is typically dysregulated during pathogenesis. While CVD research links TMAO to atherosclerotic mechanisms in vascular tissue, its molecular effects on metabolic tissues are unclear. Here we report the current standing of TMAO research in metabolic disease contexts across relevant tissues including the liver, kidney, brain, adipose, and muscle. Since poor blood glucose management is a hallmark of metabolic diseases, we also explore the variable TMAO effects on insulin resistance and insulin production. Among metabolic tissues, hepatic TMAO research is the most common, whereas its effects on other tissues including the insulin producing pancreatic β-cells are largely unexplored. Studies on diseases including obesity, diabetes, liver diseases, chronic kidney disease, and cognitive diseases reveal that TMAO effects are unique under pathologic conditions compared to healthy controls. We conclude that molecular TMAO effects are highly context-dependent and call for further research to clarify the deleterious and beneficial molecular effects observed in metabolic disease research.


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