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Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease
Open accessAbstract
Metabolomics studies hold promise for the discovery of pathways linked to disease processes. Cardiovascular disease (CVD) represents the leading cause of death and morbidity worldwide. Here we used a metabolomics approach to generate unbiased small-molecule metabolic profiles in plasma that predict risk for CVD. Three metabolites of the dietary lipid phosphatidylcholine--choline, trimethylamine N-oxide (TMAO) and betaine--were identified and then shown to predict risk for CVD in an independent large clinical cohort. Dietary supplementation of mice with choline, TMAO or betaine promoted upregulation of multiple macrophage scavenger receptors linked to atherosclerosis, and supplementation with choline or TMAO promoted atherosclerosis. Studies using germ-free mice confirmed a critical role for dietary choline and gut flora in TMAO production, augmented macrophage cholesterol accumulation and foam cell formation. Suppression of intestinal microflora in atherosclerosis-prone mice inhibited dietary-choline-enhanced atherosclerosis. Genetic variations controlling expression of flavin monooxygenases, an enzymatic source of TMAO, segregated with atherosclerosis in hyperlipidaemic mice. Discovery of a relationship between gut-flora-dependent metabolism of dietary phosphatidylcholine and CVD pathogenesis provides opportunities for the development of new diagnostic tests and therapeutic approaches for atherosclerotic heart disease.
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In the citing paper
“The mechanism by which TMAO induces stroke is not well understood; however, it is widely established that the TMAO pathway promotes the development of atherosclerosis and thrombosis.11,26,27”
From Association of L-α Glycerylphosphorylcholine With Subsequent Stroke Risk After 10 Years (2021) · cites this paper as [11]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“First, a metabolomics study reported that dietary supplementation of mice with choline, betaine, and TMAO activates upregulation of multiple macrophage scavenger receptors and subsequent accumulation of cholesterol and foam cells.11”
From Association of L-α Glycerylphosphorylcholine With Subsequent Stroke Risk After 10 Years (2021) · cites this paper as [11]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“a growing body of evidence suggests that a high plasma choline level is associated with a high risk of cardiovascular disease via trimethylamine-N-oxide (TMAO) produced by gut microbiota from choline.”
From Association of L-α Glycerylphosphorylcholine With Subsequent Stroke Risk After 10 Years (2021) · cites this paper as [11]
Experimental — accuracy not yet measuredIn the citing paper
“Numerous recent case–control and longitudinal studies have shown a striking association between trimethylamine N‐oxide (TMAO) levels and cardiovascular disease risks in a variety of cohorts.1, 2, 3, 4, 5, 6, 7, 8, 9, 10”
From Trimethylamine N‐Oxide Promotes Vascular Inflammation Through Signaling of Mitogen‐Activated Protein Kinase and Nuclear Factor‐κB (2016) · cites this paper as [1]
In the citing paper
“TMAO is derived primarily from dietary choline and carnitine through the action of gut microbiota, which metabolize these constituents to trimethylamine (TMA).1, 11, 12 TMA is absorbed in turn and travels via the portal circulation to the liver, where it is oxidized by flavin‐containing monoxygenases, primarily FMO3, to TMAO.1, 11, 12”
From Trimethylamine N‐Oxide Promotes Vascular Inflammation Through Signaling of Mitogen‐Activated Protein Kinase and Nuclear Factor‐κB (2016) · cites this paper as [1]
In the citing paper
“In studies in mice, supplementation with dietary choline, carnitine, precarnitine (γ‐butyrobetaine), or even TMAO alone was sufficient to enhance macrophage cholesterol accumulation and atherogenic plaque formation, supporting a causal relationship.1, 2, 11”
From Trimethylamine N‐Oxide Promotes Vascular Inflammation Through Signaling of Mitogen‐Activated Protein Kinase and Nuclear Factor‐κB (2016) · cites this paper as [1]
In the citing paper
“Insights into the mechanisms through which the meta-organismal pathway responsible for TMAO production are associated with enhanced CVD risks have thus far focused on the involvement of TMAO and FMO3 in atherosclerotic plaque development, altered sterol and glucose metabolism, and changes in macrophage phenotype (Wang et al., 2011 ; Koeth et al., 2013; Miao et al., 2015 ; Shih et al., 2015; War”
From Gut Microbial Metabolite TMAO Enhances Platelet Hyperreactivity and Thrombosis Risk (2016) · cites this paper as Wang et al., 2011
In the citing paper
“circulating levels of TMAO have been shown in multiple distinct clinical studies and cohorts to be associated with CVD risks”
From Gut Microbial Metabolite TMAO Enhances Platelet Hyperreactivity and Thrombosis Risk (2016) · cites this paper as Wang et al., 2011
In the citing paper
“The TMAO meta-organismal pathway has been shown to possess numerous clinical and mechanistic links (Figure 7A) with both atherosclerotic plaque development and whole body cholesterol and sterol metabolism”
From Gut Microbial Metabolite TMAO Enhances Platelet Hyperreactivity and Thrombosis Risk (2016) · cites this paper as Wang et al., 2011
In the citing paper
“In contrast, examination of hepatic FMO enzyme activity, which is responsible for converting TMA into TMAO (Wang et al., 2011; Bennett et al., 2013), revealed no significant differences between both donor mouse strains, and among the various recipient groups post cecal microbial transplantation (Figure S6, panel B).”
From Gut Microbial Metabolite TMAO Enhances Platelet Hyperreactivity and Thrombosis Risk (2016) · cites this paper as Wang et al., 2011
In the citing paper
“Animal model studies show direct provision of TMAO within the diet is pro-atherogenic, and similarly, provision of its dietary precursors (e.g. choline, carnitine, gamma butyrobetaine) also accelerates atherosclerosis development, but only in the setting of intact gut microbiota and TMA/TMAO generation (Wang et al., 2011; Koeth et al., 2013; Koeth et al, 2014).”
From Gut Microbial Metabolite TMAO Enhances Platelet Hyperreactivity and Thrombosis Risk (2016) · cites this paper as Wang et al., 2011
In the citing paper
“recent studies reveal participation of gut microbes in a metaorganismal pathway that contributes to the development of atherosclerosis (Wang et al., 2011; Koeth et al., 2013; Tang et al., 2013; Gregory et al., 2015).”
From Gut Microbial Metabolite TMAO Enhances Platelet Hyperreactivity and Thrombosis Risk (2016) · cites this paper as Wang et al., 2011
In the citing paper
“Briefly, specific trimethylamine (TMA) containing dietary nutrients, such as phosphatidylcholine, choline, and carnitine, can be used by gut microbes as a carbon fuel source. A waste product produced is TMA, which is carried via the portal circulation to the liver where it is rapidly converted by a family of enzymes, host hepatic flavin monooxygenases (FMOs), into TMA N-oxide (TMAO) (Wang et al.,”
From Gut Microbial Metabolite TMAO Enhances Platelet Hyperreactivity and Thrombosis Risk (2016) · cites this paper as Wang et al., 2011
In the citing paper
“Finally, an association between plasma TMAO levels and both the extent of coronary atherosclerotic plaque burden and CVD risks has been observed in multiple distinct clinical studies (Wang et al., 2011; Tang et al., 2013; Tang et al., 2014; Lever et al., 2014; Tang et al., 2015).”
From Gut Microbial Metabolite TMAO Enhances Platelet Hyperreactivity and Thrombosis Risk (2016) · cites this paper as Wang et al., 2011
In the citing paper
“Specifically, gut microbiota-mediated metabolism of phosphatidylcholine, choline or L-carnitine each have been shown to ultimately produced trimethylamine-N-oxide (TMAO), and in multiple clinical studies, TMAO levels have been shown to be associated with cardiovascular risks8–10, 13.”
In the citing paper
“Animal model and human clinical studies demonstrate an obligatory role for gut microbiota in TMAO formation from TMA-containing nutrients including choline and phosphatidylcholine9, 10, L-carnitine8, and more recently, γ-butyrobetaine15, and to a lesser degree, the choline oxidation metabolite betaine11.”
In the citing paper
“in multiple clinical studies, TMAO levels have been shown to be associated with cardiovascular risks8–10, 13.”
In the citing paper
“Trimethylamine-N-oxide (TMAO) levels were determined by stable isotope dilution high-performance liquid chromatography with online electrospray ionization tandem mass spectrometry (LC/MS/MS) on an AB SCIEX 5500 triple quadrupole mass spectrometer (AB SCIEX, Framingham MA) using d9-(trimethyl)-labeled internal standards as previously described10, 21.”
In the citing paper
“Of note, however, compared with comparable oral challenge of d9-choline, 14 betaine was a far poorer precursor for TMAO, as it produced 100-fold less d9-TMAO (Figure 3A and B).”
From Prognostic value of choline and betaine depends on intestinal microbiota-generated metabolite trimethylamine-N-oxide (2014) · cites this paper as [14]
In the citing paper
“Moreover, systemic levels of choline, betaine, and TMAO each are independently associated with the prevalence of CVD. 14”
From Prognostic value of choline and betaine depends on intestinal microbiota-generated metabolite trimethylamine-N-oxide (2014) · cites this paper as [14]
In the citing paper
“Choline, betaine, and TMAO are all metabolites formed following ingestion of dietary PC. 14,17”
From Prognostic value of choline and betaine depends on intestinal microbiota-generated metabolite trimethylamine-N-oxide (2014) · cites this paper as [14]
In the citing paper
“Gut microbiota have been shown to play an obligate role in TMAO formation from ingested choline, PC, and carnitine in both animal models and humans.14,16”
From Prognostic value of choline and betaine depends on intestinal microbiota-generated metabolite trimethylamine-N-oxide (2014) · cites this paper as [14]
In the citing paper
“Moreover, elevated levels of TMAO have been shown to predict increased prevalent cardiovascular disease (CVD) risk, and increased incident risk of major adverse cardiovascular events (MACE ¼ myocardial infarction, stroke, and death) in large-scale human clinical studies.14,16,17”
From Prognostic value of choline and betaine depends on intestinal microbiota-generated metabolite trimethylamine-N-oxide (2014) · cites this paper as [14]
In the citing paper
“TMAO formation in mammals occurs via a two-step metaorganismal pathway”
From Non-lethal Inhibition of Gut Microbial Trimethylamine Production for the Treatment of Atherosclerosis (2015) · cites this paper as Wang et al., 2011
In the citing paper
“both enhances atherosclerosis in animal models”
From Non-lethal Inhibition of Gut Microbial Trimethylamine Production for the Treatment of Atherosclerosis (2015) · cites this paper as Wang et al., 2011
In the citing paper
“choline, phosphatidylcholine and carnitine, trimethylamine (TMA)-containing nutrients abundant in foods like meat, egg yolk and high fat dairy products, serve as dietary precursors for trimethylamine N-oxide (TMAO) generation in mice and humans”
From Non-lethal Inhibition of Gut Microbial Trimethylamine Production for the Treatment of Atherosclerosis (2015) · cites this paper as Wang et al., 2011
In the citing paper
“Anaerobic choline degradation is believed to serve as the major source of TMA formation within the intestines”
From Non-lethal Inhibition of Gut Microbial Trimethylamine Production for the Treatment of Atherosclerosis (2015) · cites this paper as Wang et al., 2011
In the citing paper
“As was previously observed (Wang et al., 2011), a choline-enriched diet promoted marked increase in endogenous macrophage foam cell generation (approximately 2-fold on choline-supplemented diet; p=0.02)”
From Non-lethal Inhibition of Gut Microbial Trimethylamine Production for the Treatment of Atherosclerosis (2015) · cites this paper as Wang et al., 2011
In the citing paper
“Changes in bacterial composition have been shown to serve as a primary driver of TMAO levels in other studies (10,15).”
From Prognostic Value of Elevated Levels of Intestinal Microbe-Generated Metabolite Trimethylamine-N-Oxide in Patients With Heart Failure (2014) · cites this paper as [10]
In the citing paper
“While TMAO has been shown to possess pro-atherogenic properties (10,11,17)”
From Prognostic Value of Elevated Levels of Intestinal Microbe-Generated Metabolite Trimethylamine-N-Oxide in Patients With Heart Failure (2014) · cites this paper as [10]
In the citing paper
“Our group has recently described a mechanistic link between intestinal microbe-dependent generation of trimethylamine-N-oxide (TMAO) and increased risk for future cardiovascular events (death, myocardial infarction, and stroke) by a pathway involving dietary nutrients such as phosphatidylcholine, choline, and carnitine (10,11).”
From Prognostic Value of Elevated Levels of Intestinal Microbe-Generated Metabolite Trimethylamine-N-Oxide in Patients With Heart Failure (2014) · cites this paper as [10]
In the citing paper
“Specifically, gut microbial metabolism of phosphatidylcholine, the major dietary source of choline, was first shown to produce a proatherogenic metabolite, trimethylamine-N-oxide (TMAO), via initial formation of trimethylamine (TMA), followed by host hepatic flavin monooxygenase mediated conversion to TMAO (Wang et al., 2011) (Figure S1; Gut Pathway1).”
From γ-Butyrobetaine Is a Proatherogenic Intermediate in Gut Microbial Metabolism of L-Carnitine to TMAO (2014) · cites this paper as Wang et al., 2011
In the citing paper
“multiple human studies with distinct clinical populations have now confirmed a strong association between plasma TMAO levels and cardiovascular disease risks (Koeth et al., 2013; Tang et al., 2013; Tang WHW, (2014); Wang et al., 2011; Wang et al., 2014)”
From γ-Butyrobetaine Is a Proatherogenic Intermediate in Gut Microbial Metabolism of L-Carnitine to TMAO (2014) · cites this paper as Wang et al., 2011
In the citing paper
“Our group recently discovered that certain dietary nutrients possessing a trimethylamine (TMA) moiety, namely choline/ phosphatidylcholine and L-carnitine, participate in the development of atherosclerotic heart disease.”
From The contributory role of gut microbiota in cardiovascular disease (2014) · cites this paper as [25]
In the citing paper
“a metabolite shown to be both mechanistically linked to atherosclerosis and whose levels are strongly linked to cardiovascular disease (CVD) risks.”
From The contributory role of gut microbiota in cardiovascular disease (2014) · cites this paper as [25]
In the citing paper
“A meta-organismal pathway was elucidated involving gut microbiota-dependent formation of TMA and host hepatic flavin monooxygenase 3dependent (FMO3-dependent) formation of TMA-N-oxide (TMAO), a metabolite shown to be both mechanistically linked to atherosclerosis and whose levels are strongly linked to cardiovascular disease (CVD) risks.”
From The contributory role of gut microbiota in cardiovascular disease (2014) · cites this paper as [25]
In the citing paper
“TMAO has been shown to affect cholesterol and sterol metabolism in animal models, enhancing macrophage cholesterol accumulation and atherosclerosis development.”
From The contributory role of gut microbiota in cardiovascular disease (2014) · cites this paper as [25]
In the citing paper
“In multiple human studies, elevated TMAO has been independently associated with prevalent CVD and incident risks for MI, stroke, death, and revascularization.”
From The contributory role of gut microbiota in cardiovascular disease (2014) · cites this paper as [25]
In the citing paper
“While plasma levels of all 3 metabolites (choline, betaine, and TMAO) identified in the original metabolomics study are associated with increased risk of CVD phenotypes in subjects presenting for cardiac risk evaluation (n = 1,876) (25), subsequent analyses in larger cohorts revealed that the prognostic value was largely confined to the formation of TMAO, especially from choline and L-carnitine (”
From The contributory role of gut microbiota in cardiovascular disease (2014) · cites this paper as [25]
In the citing paper
“These observations highlight the obligatory role of intestinal microbiota in the generation of TMAO from multiple dietary nutrients, and TMAO as the proatherogenic species likely promoting the striking associations noted between plasma levels and both prevalent and incident CVD risks.”
From The contributory role of gut microbiota in cardiovascular disease (2014) · cites this paper as [25]
In the citing paper
“Moreover, enhanced protein surface levels were observed of previously implicated scavenger receptors (CD36 and SR-A1) on macrophages involved in cholesterol accumulation and foam cell formation (25).”
From The contributory role of gut microbiota in cardiovascular disease (2014) · cites this paper as [25]
In the citing paper
“TMAO supplementation of apolipoprotein E-null mice was observed to foster enhanced macrophage foam cell formation in both the artery wall and the peritoneal cavity, as well as to promote aortic root atherosclerotic plaque development (25).”
From The contributory role of gut microbiota in cardiovascular disease (2014) · cites this paper as [25]
In the citing paper
“a metabolite shown to be both mechanistically linked to atherosclerosis and whose levels are strongly linked to cardiovascular disease (CVD) risks.”
From The contributory role of gut microbiota in cardiovascular disease (2014) · cites this paper as [25]
In the citing paper
“An obligatory role for gut microbiota in both TMA and TMAO formation from ingested PC was confirmed in animal model studies, which included germ-free mice (25), as well as human clinical investigations involving ingestion of egg yolk, isotope-labeled PC, and a cocktail of oral antibiotics (37).”
From The contributory role of gut microbiota in cardiovascular disease (2014) · cites this paper as [25]
In the citing paper
“In both humans and mice, hepatic FMO3 expression was observed to be reduced in males compared with females (25,54) and could be induced by dietary bile acids through a mechanism that involves FXR (54).”
From The contributory role of gut microbiota in cardiovascular disease (2014) · cites this paper as [25]
In the citing paper
“Our laboratory has elucidated a link between intestinal microbiota, dietary trimethylamine-containing nutrients ( e.g. choline, phosphatidylcholine, and carnitine), andcardiovasculardisease(5-7).”
From Transmission of Atherosclerosis Susceptibility with Gut Microbial Transplantation (2015) · cites this paper as [5]
In the citing paper
“phosphatidylcholine, the major dietary source of choline, and the gut microbe-dependent metabolite, trimethylamine N -oxide (TMAO), 4 are both mechanistically linked to atherosclerosis development (5, 6, 8)”
From Transmission of Atherosclerosis Susceptibility with Gut Microbial Transplantation (2015) · cites this paper as [5]
In the citing paper
“plasma levels in subjects are associated with prevalent and incident cardiovascular disease risks (5, 7, 9, 10).”
From Transmission of Atherosclerosis Susceptibility with Gut Microbial Transplantation (2015) · cites this paper as [5]
In the citing paper
“An obligatory role for gut microbes in TMAO formation in both mice (5, 6) and humans (7) was shown”
From Transmission of Atherosclerosis Susceptibility with Gut Microbial Transplantation (2015) · cites this paper as [5]
In the citing paper
“both dietary choline-induced and carnitine-induced enhancement in atherosclerosis in mice is prevented by suppression of gut microbes (and TMAO formation) with poorly absorbed broad spectrum oral antibiotics (5, 6).”
From Transmission of Atherosclerosis Susceptibility with Gut Microbial Transplantation (2015) · cites this paper as [5]
In the citing paper
“no studies to date have directly demonstrated transmission of atherosclerosis susceptibility by gut microbial transplantation.”
From Transmission of Atherosclerosis Susceptibility with Gut Microbial Transplantation (2015) · cites this paper as [5]
In the citing paper
“The microbial-derived metabolite trimethylamine N-oxide (TMAO) has been implicated in metabolic [5], cardiovascular [6, 7], and cerebrovascular [8] disease.”
From The gut microbiota-derived metabolite trimethylamine N-oxide is elevated in Alzheimer’s disease (2018) · cites this paper as [6]
In the citing paper
“Trimethylamine N-oxide (TMAO) is a gut microbiota-generated metabolite with mechanistic links to the pathogenesis of atherosclerotic heart disease.[1][2][3][4][5]”
From Impact of chronic dietary red meat, white meat, or non-meat protein on trimethylamine N-oxide metabolism and renal excretion in healthy men and women (2019) · cites this paper as [1]
In the citing paper
“Elevated plasma TMAO levels are observed in subjects at risk for incident cardiovascular disease (CVD) development and adverse CVD events including heart attack, stroke, and death.[1][2][3][4]”
From Impact of chronic dietary red meat, white meat, or non-meat protein on trimethylamine N-oxide metabolism and renal excretion in healthy men and women (2019) · cites this paper as [1]
In the citing paper
“Trimethylamine N-oxide is generated via a metaorganismal pathway that begins with gut microbiota-dependent formation of trimethylamine (TMA) from TMA containing nutrient precursors (Figure 1A).[1][2][3]16”
From Impact of chronic dietary red meat, white meat, or non-meat protein on trimethylamine N-oxide metabolism and renal excretion in healthy men and women (2019) · cites this paper as [1]
In the citing paper
“Consequently, a diet enriched in meat, particularly red meat, has higher content of both choline and carnitine nutrient precursors for TMA and TMAO generation.1,3”
From Impact of chronic dietary red meat, white meat, or non-meat protein on trimethylamine N-oxide metabolism and renal excretion in healthy men and women (2019) · cites this paper as [1]
In the citing paper
“Beyond choline and carnitine, potential nutrient precursors for TMA production have been reported, including the carnitine related metabolites c-butyrobetaine and crotonobetaine, and the choline oxidation product betaine.1,16,19”
From Impact of chronic dietary red meat, white meat, or non-meat protein on trimethylamine N-oxide metabolism and renal excretion in healthy men and women (2019) · cites this paper as [1]
In the citing paper
“Some of these TMA containing compounds can participate in TMA/TMAO formation in a gut microbiota-dependent manner, and also be generated by gut microbiota metabolism of L-carnitine.1,3,16,19”
From Impact of chronic dietary red meat, white meat, or non-meat protein on trimethylamine N-oxide metabolism and renal excretion in healthy men and women (2019) · cites this paper as [1]
In the citing paper
“One potential candidate for this is the metaorganismal TMAO pathway.1,14,15”
From Impact of chronic dietary red meat, white meat, or non-meat protein on trimethylamine N-oxide metabolism and renal excretion in healthy men and women (2019) · cites this paper as [1]
In the citing paper
“studies suggesting an association between high plasma TMAO levels and risk for developing atherosclerosis have increased markedly [7,13,14,15,16,17]”
From Implication of Trimethylamine N-Oxide (TMAO) in Disease: Potential Biomarker or New Therapeutic Target (2018) · cites this paper as [7]
In the citing paper
“In humans, recent clinical studies evidence a positive correlation between elevated plasma levels of TMAO and an increased risk for major adverse cardiovascular events.”
From Implication of Trimethylamine N-Oxide (TMAO) in Disease: Potential Biomarker or New Therapeutic Target (2018) · cites this paper as [7]
In the citing paper
“some studies performed with antibiotics in rats and humans reveal that the production of TMA and TMAO is almost totally suppressed with the use of broad-spectrum antibiotics, such as Ciprofloxacin, Vancomycin or Metronidazole. However, the levels of TMAO return to normal after one month of the withdrawal of the antibiotics [7,52].”
From Implication of Trimethylamine N-Oxide (TMAO) in Disease: Potential Biomarker or New Therapeutic Target (2018) · cites this paper as [7]
In the citing paper
“In this context, it is thought that TMAO could serve as a biomarker in humans to predict prevalence of CVD and increased incidence of major adverse cardiovascular events (MACE), such as myocardial infarction, stroke and even death [7,14,52,53,54,55].”
From Implication of Trimethylamine N-Oxide (TMAO) in Disease: Potential Biomarker or New Therapeutic Target (2018) · cites this paper as [7]
In the citing paper
“Indeed, elevated plasma TMAO levels have been found in people at risk of CVD. These patients usually show greater concentrations of the TMAO precursors too.”
From Implication of Trimethylamine N-Oxide (TMAO) in Disease: Potential Biomarker or New Therapeutic Target (2018) · cites this paper as [7]
In the citing paper
“Additionally, TMAO increases the expression in macrophages of scavenger receptors CD36 and SR-A1, which promote lipid accumulation and foam cell formation [7,17].”
From Implication of Trimethylamine N-Oxide (TMAO) in Disease: Potential Biomarker or New Therapeutic Target (2018) · cites this paper as [7]
In the citing paper
“Some investigations revealed that TMAO alters cholesterol and sterol metabolism in various compartments, including the bile acid compartment [7,14,15].”
From Implication of Trimethylamine N-Oxide (TMAO) in Disease: Potential Biomarker or New Therapeutic Target (2018) · cites this paper as [7]
In the citing paper
“Plasma TMAO levels were supressed and macrophage foam cell formation was inhibited [7].”
From Implication of Trimethylamine N-Oxide (TMAO) in Disease: Potential Biomarker or New Therapeutic Target (2018) · cites this paper as [7]
In the citing paper
“Other studies performed in mice using a mix of vancomycin, neomycin-sulphate, metronidazole and ampicillin, showed an inhibition of dietary choline-enhanced atherosclerosis.”
From Implication of Trimethylamine N-Oxide (TMAO) in Disease: Potential Biomarker or New Therapeutic Target (2018) · cites this paper as [7]
In the citing paper
“Plasma TMAO levels were supressed and macrophage foam cell formation was inhibited [7].”
From Implication of Trimethylamine N-Oxide (TMAO) in Disease: Potential Biomarker or New Therapeutic Target (2018) · cites this paper as [7]
In the citing paper
“Elevated TMAO has been observed in patients with cardiovascular disease and atherosclerosis, highlighting a potential downside to increased protein intake.[15-17,22, 37]”
From The microbiome of professional athletes differs from that of more sedentary subjects in composition and particularly at the functional metabolic level (2018) · cites this paper as [22]
In the citing paper
“Recent studies by Wang and Tang et al reported that circulating concentrations of trimethylamine N‐oxide (TMAO), a metabolite derived from the gut microbiota, were predictive of prevalent cardiovascular diseases (CVDs)1 and future cardiovascular events3 in clinical cohorts.”
In the citing paper
“TMAO is a small organic compound, mainly derived from choline (found in foods such as red meat, fish, poultry, and eggs), which is metabolized to produce trimethylamine (TMA) by microbiota1, 4 and then to TMAO by the hepatic enzyme, flavin monooxygenase 3.1, 5”
In the citing paper
“TMAO was also found to promote the development of atherosclerosis in animal models, providing the first link between dietary lipid intake, the intestinal microbiota, and the risk for the development of atherosclerosis57.”
From Diet and the Intestinal Microbiome: Associations, Functions, and Implications for Health and Disease (2014) · cites this paper as [57]
In the citing paper
“The intestinal microbiota may also contribute to development of atherosclerosis by producing metabolites of the dietary lipid phosphatidylcholine that are associated with the risk for coronary vascular disease.”
From Diet and the Intestinal Microbiome: Associations, Functions, and Implications for Health and Disease (2014) · cites this paper as [57]
In the citing paper
“Wang et al. identified a novel pathway linking dietary lipid intake, the intestinal microbiota, and atherosclerosis (Figure 3)57, 58.”
From Diet and the Intestinal Microbiome: Associations, Functions, and Implications for Health and Disease (2014) · cites this paper as [57]
In the citing paper
“Catabolism of choline by the intestinal microbiota results in the formation of the gas, trimethylamine (TMA), which is metabolized by the liver into trimethylamine oxide (TMAO)—a small molecule that is strongly associated with the increased risk for coronary vascular disease in humans.”
From Diet and the Intestinal Microbiome: Associations, Functions, and Implications for Health and Disease (2014) · cites this paper as [57]
In the citing paper
“Even though high concentrations of circulating plasma TMAO increase cholesterol influx to peritoneal macrophages (118), cholesterol efflux or cholesterol biosynthesis appears to be unchanged.”
From Trimethylamine N -Oxide, the Microbiome, and Heart and Kidney Disease (2017) · cites this paper as [118]
In the citing paper
“Transcript levels of hepatic bile acid transporters, such as Oatp1, Oatp4, Mrp2, and Ntcp, also showed significant reductions in response to TMAO feeding (118).”
From Trimethylamine N -Oxide, the Microbiome, and Heart and Kidney Disease (2017) · cites this paper as [118]
In the citing paper
“Dietary supplementation of TMAO also decreased intestinal cholesterol absorption.The effect is consistent with reduced expression of the cholesterol transporter Niemann-Pick C1-like 1 but again does not explain reductions in RCT (118).”
From Trimethylamine N -Oxide, the Microbiome, and Heart and Kidney Disease (2017) · cites this paper as [118]
In the citing paper
“The proatherogenic effects of choline, γ-butyrobetaine, and carnitine were prevented by treatment with antibiotics, suggesting that microbial metabolism of these precursors was required for the effect (63, 118).”
From Trimethylamine N -Oxide, the Microbiome, and Heart and Kidney Disease (2017) · cites this paper as [118]
In the citing paper
“TMAO feeding did not change the expression of hepatic cholesterol exporters, but striking reductions in bile acid pool size and species, along with reduced expression of the cytochrome P450 family of enzymes, Cyp7a1 and Cyp27a1, were noted (118).”
From Trimethylamine N -Oxide, the Microbiome, and Heart and Kidney Disease (2017) · cites this paper as [118]
In the citing paper
“In fact, modest but significant increases in many cholesterol transporters, such as Abca1 and Abcg1, were noted (118).”
From Trimethylamine N -Oxide, the Microbiome, and Heart and Kidney Disease (2017) · cites this paper as [118]
In the citing paper
“The proatherogenic effects of choline, γ-butyrobetaine, and carnitine were prevented by treatment with antibiotics, suggesting that microbial metabolism of these precursors was required for the effect (63, 118).”
From Trimethylamine N -Oxide, the Microbiome, and Heart and Kidney Disease (2017) · cites this paper as [118]
In the citing paper
“Atherosclerosis-prone mice (C57BL/6J Apo e -/-) fed a normal diet supplemented with additional choline (118) and L-carnitine (63) or TMAO (118) had increased total aortic root atherosclerotic plaque area compared with mice fed a control diet (118).”
From Trimethylamine N -Oxide, the Microbiome, and Heart and Kidney Disease (2017) · cites this paper as [118]
In the citing paper
“These macrophages had excess cholesterol accumulation and foam cell formation (118).”
From Trimethylamine N -Oxide, the Microbiome, and Heart and Kidney Disease (2017) · cites this paper as [118]
In the citing paper
“Peritoneal macrophages obtained from C57BL/6J mice, fed a TMAO-supplemented diet for more than three weeks, showed increased mRNA levels of two macrophage scavenger receptors (CD36 and SR-A1), which are implicated in atherosclerosis (118).”
From Trimethylamine N -Oxide, the Microbiome, and Heart and Kidney Disease (2017) · cites this paper as [118]
In the citing paper
“a link between dietary phosphatidylcholine, a nutrient common in a Western diet, gut microbiota-dependent generation of the metabolite trimethylamine N-oxide (TMAO), and cardiovascular disease (CVD) pathogenesis, was first described7.”
From Development of a gut microbe–targeted nonlethal therapeutic to inhibit thrombosis potential (2018) · cites this paper as [7]
In the citing paper
“Trimethylamine-N-oxide (TMAO), a microbiota-dependent metabolite derived from trimethylamine (TMA)-containing nutrients that are abundant in a Western diet”
From Development of a gut microbe–targeted nonlethal therapeutic to inhibit thrombosis potential (2018) · cites this paper as [7]
In the citing paper
“A recent metabolomics approach identified that plasma trimethylamine-N-oxide (TMAO), a choline metabolite, is a novel and independent risk factor for promoting AS (2, 3).”
In the citing paper
“TMAO has been shown to induce AS by affecting cholesterol metabolism through inhibiting hepatic bile acid (BA) synthesis (2–4).”
In the citing paper
“TMAO appears to contribute to the development of AS, in part by affecting cholesterol metabolism through the regulation of the BA synthesis pathway (4).”
In the citing paper
“Enhanced AS, as observed by dietary choline supplementation, is entirely dependent on the gut microbiota.”
In the citing paper
“Recently, plasma TMAO was identified as a metabolite strongly associated with AS (2–4).”
In the citing paper
“Treatment with Abs, or germ-free conditions, abolished dietary choline-driven TMAO generation and the development of AS (2, 4).”
In the citing paper
“Researchers confirmed that feeding AS-prone mice diets enriched in either choline or TMAO enhanced the development of AS.”
In the citing paper
“Previous studies suggest that TMAO partially contributes to the development of AS by regulating the major pathway of cholesterol metabolism and the bile acid synthetic pathway.4, 5, 6”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [4]
In the citing paper
“Trimethylamine‐N‐oxide (TMAO) has recently been identified as a novel and independent risk factor for promoting atherosclerosis through inducing vascular inflammation.”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [4]
In the citing paper
“Researchers have confirmed that TMAO contributes to the development of AS, in part, by affecting cholesterol metabolism through regulating the major pathway for cholesterol elimination from the body and the bile acid synthetic pathway at multiple levels.4, 6”
From Trimethylamine‐N‐Oxide Induces Vascular Inflammation by Activating the NLRP3 Inflammasome Through the SIRT3‐SOD2‐mtROS Signaling Pathway (2017) · cites this paper as [4]
In the citing paper
“Hazen and coworkers showed that consumption of foods rich in choline or carnitine, such as eggs, milk, liver, meat, or fish, produced high concentrations of TMAO in both humans and animals who possessed the requisite microbiota for metabolizing choline or carnitine to trimethylamine, the immediate precursor of TMAO (108, 171, 172).”
From The food metabolome: a window over dietary exposure (2014) · cites this paper as [171]
In the citing paper
“In their initial untargeted LC-MS/MS investigation (171), the authors showed that the nutrient choline, along with its major metabolites, betaine and TMAO, were associated with risks of cardiovascular disease, particularly TMAO.”
From The food metabolome: a window over dietary exposure (2014) · cites this paper as [171]
In the citing paper
“These observations are of interest because high TMAO levels linked to TMA oxidation by the human hepatic flavin monooxygenase FMO3 have been associated with cardiovascular diseases (CVDs) (Tang et al., 2013; Wang et al., 2011), while it is known that RYGB is associated with a lower CVD risk (Sjöström et al., 2012).”
From Roux-en-Y Gastric Bypass and Vertical Banded Gastroplasty Induce Long-Term Changes on the Human Gut Microbiome Contributing to Fat Mass Regulation (2015) · cites this paper as Wang et al., 2011
In the citing paper
“Recent human studies have established that the levels of TMAO in serum are positively correlated with impaired renal function, colorectal cancer, and cardiovascular disease (CVD) (8, 10, 17, 18).”
From Intestinal Microbiota Composition Modulates Choline Bioavailability from Diet and Accumulation of the Proatherogenic Metabolite Trimethylamine- N -Oxide (2015) · cites this paper as [8]
In the citing paper
“Recent human studies have established that the levels of TMAO in serum are positively correlated with impaired renal function, colorectal cancer, and cardiovascular disease (CVD) (8, 10, 17, 18).”
From Intestinal Microbiota Composition Modulates Choline Bioavailability from Diet and Accumulation of the Proatherogenic Metabolite Trimethylamine- N -Oxide (2015) · cites this paper as [8]
In the citing paper
“TMAO exacerbates atherosclerosis in a genetic knockout mouse model, in part by promoting forward cholesterol transport and by inhibiting reverse cholesterol transport (8, 10, 19, 20).”
From Intestinal Microbiota Composition Modulates Choline Bioavailability from Diet and Accumulation of the Proatherogenic Metabolite Trimethylamine- N -Oxide (2015) · cites this paper as [8]
In the citing paper
“TMAO exacerbates atherosclerosis in a genetic knockout mouse model, in part by promoting forward cholesterol transport and by inhibiting reverse cholesterol transport (8, 10, 19, 20).”
From Intestinal Microbiota Composition Modulates Choline Bioavailability from Diet and Accumulation of the Proatherogenic Metabolite Trimethylamine- N -Oxide (2015) · cites this paper as [8]
In the citing paper
“Once TMA is absorbed by the host, it is further metabolized by flavin monooxygenases 1 and 3 (FMO1 and FMO3) in the host liver to generate trimethylamine-N-oxide (TMAO) (8, 15, 16).”
From Intestinal Microbiota Composition Modulates Choline Bioavailability from Diet and Accumulation of the Proatherogenic Metabolite Trimethylamine- N -Oxide (2015) · cites this paper as [8]
In the citing paper
“TMAO exacerbates atherosclerosis in a genetic knockout mouse model, in part by promoting forward cholesterol transport and by inhibiting reverse cholesterol transport (8, 10, 19, 20).”
From Intestinal Microbiota Composition Modulates Choline Bioavailability from Diet and Accumulation of the Proatherogenic Metabolite Trimethylamine- N -Oxide (2015) · cites this paper as [8]
In the citing paper
“Recent human studies have established that the levels of TMAO in serum are positively correlated with impaired renal function, colorectal cancer, and cardiovascular disease (CVD) (8, 10, 17, 18).”
From Intestinal Microbiota Composition Modulates Choline Bioavailability from Diet and Accumulation of the Proatherogenic Metabolite Trimethylamine- N -Oxide (2015) · cites this paper as [8]
In the citing paper
“Likewise, gut microbes can also convert otherwise beneficial dietary compounds, such as choline, into metabolites that are detrimental to human health (7–10).”
From Intestinal Microbiota Composition Modulates Choline Bioavailability from Diet and Accumulation of the Proatherogenic Metabolite Trimethylamine- N -Oxide (2015) · cites this paper as [8]
In the citing paper
“consistent with previous studies in conventionally raised mice which demonstrated that FMO3 is expressed at higher levels in females than in males (8, 27).”
From Intestinal Microbiota Composition Modulates Choline Bioavailability from Diet and Accumulation of the Proatherogenic Metabolite Trimethylamine- N -Oxide (2015) · cites this paper as [8]
In the citing paper
“a metabolite linked to accumulation of cholesterol in macrophages and foam cell deposition127, and higher risk of a major adverse cardiac event128.”
From The microbial pharmacists within us: a metagenomic view of xenobiotic metabolism (2016) · cites this paper as [127]
In the citing paper
“In the colon, choline-containing compounds undergo metabolism by microbial glycyl radical enzymes126 to form the intermediate gas trimethylamine (TMA; Fig. 4). In turn, TMA is absorbed and oxidized by hepatic flavin monooxygenases, forming TMA N-oxide (TMAO)”
From The microbial pharmacists within us: a metagenomic view of xenobiotic metabolism (2016) · cites this paper as [127]
In the citing paper
“and by reinforcing cholesterol accumulation in macrophages and foam cell formation.186”
From Interaction between microbiota and immunity in health and disease (2020) · cites this paper as [186]
In the citing paper
“TMAO augments arthrosclerosis by upregulating the macrophage scavenger receptors CD36 and SR-A1”
From Interaction between microbiota and immunity in health and disease (2020) · cites this paper as [186]
In the citing paper
“a series of recent studies [68-70] revealed a link between microbiota and atherogenesis.”
From Antibiotic-Induced Changes in the Intestinal Microbiota and Disease (2016) · cites this paper as [69]
In the citing paper
“LC- or PC- supplemented diets were found to induce higher atheroma formation and wider aortic lesions in ApoE- mice, and disease was ameliorated by antibiotic treatment [68, 69].”
From Antibiotic-Induced Changes in the Intestinal Microbiota and Disease (2016) · cites this paper as [69]
In the citing paper
“Dietary phosphatydilcholine (PC), a lipid broadly present in foods, and L-carnitine (LC), a molecule abundant in red meat, are transformed by the microbiota into pro-atherogenic trimethylamine (TMA).”
From Antibiotic-Induced Changes in the Intestinal Microbiota and Disease (2016) · cites this paper as [69]
In the citing paper
“the production of trimethylamine (TMA) from dietary carnitine and choline (Wang et al., 2011;Koeth et al., 2013).”
From Gut reactions: Breaking down xenobiotic–microbiome interactions (2019) · cites this paper as Wang et al., 2011
In the citing paper
“excess conversion to TMA can lead to artherosclerosis as a consequence of further metabolism by host hepatic processing to TMAO (Zeisel and da Costa, 2009;Wang et al., 2011;Koeth et al., 2013;Craciun et al., 2014).”
From Gut reactions: Breaking down xenobiotic–microbiome interactions (2019) · cites this paper as Wang et al., 2011
In the citing paper
“This is exemplified by trimethylamine (TMA), a microbial metabolite that is produced by various taxa of the gut microbiota from dietary quaternary amines, mainly choline and carnitine. TMA is absorbed via the intestinal epithelium and further oxidized to trimethylamine N-oxide (TMAO), which was associated with atherosclerosis and severe cardiovascular disease in several independent studies [1–4].”
From Uncovering the trimethylamine-producing bacteria of the human gut microbiota (2017) · cites this paper as [1]
In the citing paper
“The first studies revealing a potential causal link between the gut microbiome and CVD focused on trimethylamine N-oxide (TMAO), a metaorganismal metabolite formed following ingestion of dietary nutrients abundant in a Western diet (e.g. lecithin, choline, carnitine)7–9.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [9]
In the citing paper
“Through these and other studies, generation of TMAO in humans and mice has been shown to occur via a multistep, metaorganismal pathway starting with the dietary precursors choline9, phosphatidylcholine8, 9, and carnitine7.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [9]
In the citing paper
“Almost a decade ago, Wang et al. first causally linked gut microbiota with oral intake of nutrient precursors, TMAO production, and CVD risk (Figures 1 and 2)9.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [9]
In the citing paper
“First, the gut microbial community composition is critical since there is an initial obligatory role of gut microbes in TMA(O) generation7, 9.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [9]
In the citing paper
“Several analytes linked to phosphatidylcholine metabolism, including TMAO, were identified, and TMAO was shown to both predict CVD risks in multiple clinical cohorts, and facilitate accelerated atherosclerosis (as did nutrient precursors with an intact host gut microbiome) in animal models9.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [9]
In the citing paper
“TMAO has been shown to enhance atherosclerosis in most, but not all, mechanistic and animal model studies7, 9, 78–82.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [9]
In the citing paper
“The TMA produced is then transported to liver via the portal vein and readily metabolized by host hepatic flavin monooxygenases (FMOs) (mainly FMO376) into TMAO9.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [9]
In the citing paper
“In atherosclerosis-prone ApoE−/− mice, dietary supplementation with choline led to augmented atherosclerotic lesion burden, higher aortic expression of scavenger receptors (CD36 and scavenger receptor A), increased cholesterol laden macrophage foam cell formation9, and impaired in vivo reverse cholesterol transport7.”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [9]
In the citing paper
“Rodents show a significant sexual dimorphism with respect to FMO3 expression, and TMAO levels, with females showing higher levels (and greater atherosclerosis capacity9, 76).”
From Gut microbiota and cardiovascular disease. (2020) · cites this paper as [9]
In the citing paper
“Using a metabolomics approach, Wang et al. discovered a cluster of three phospholipid-associated molecules choline, betaine, and TMAO, associated with atherosclerosis [32].”
From Trimethylamine N-oxide: the good, the bad and the unknown. (2016) · cites this paper as [32]
In the citing paper
“Further studies in a murine model of atherosclerosis demonstrated that plasma TMAO levels in apoE−/− mice positively correlated with atheroma burden [32].”
From Trimethylamine N-oxide: the good, the bad and the unknown. (2016) · cites this paper as [32]
In the citing paper
“Wang et al. showed that diet containing choline, TMAO or betaine could enhance up-regulation of multiple macrophage scavenger receptors that are linked to atherosclerosis [32,38].”
From Trimethylamine N-oxide: the good, the bad and the unknown. (2016) · cites this paper as [32]
In the citing paper
“Systemic levels of trimethylamine N-oxide (TMAO), a pro-atherogenic and pro-thrombotic metabolite produced from gut microbiota metabolism of dietary trimethylamine (TMA)-containing nutrients such as choline or carnitine, predict incident cardiovascular event risks in stable primary and secondary prevention subjects.”
In the citing paper
“Trimethylamine N-oxide exerts pro-atherosclerotic effects via a variety of effects, including changes in macrophage and tissue sterol metabolism, and endothelial cell activation 1,3,23 .”
In the citing paper
“a metabolomics analysis shows that metabolism of dietary phosphatidylcholine by gut microbiota produces proatherogenic trimethylamine-N-oxide, which can accelerate atherosclerosis in mice.17,18”
From Akkermansia Muciniphila Protects Against Atherosclerosis by Preventing Metabolic Endotoxemia-Induced Inflammation in Apoe −/− Mice (2016) · cites this paper as [17]
In the citing paper
“Several recent studies have identified trimethylamine N-oxide, a metabolite of the gut microbiota, as an independent risk factor for cardiovascular disease.17,18,34”
From Akkermansia Muciniphila Protects Against Atherosclerosis by Preventing Metabolic Endotoxemia-Induced Inflammation in Apoe −/− Mice (2016) · cites this paper as [17]
In the citing paper
“Trimethylamine (TMA) and TMA N-oxide, which are gut microbiota metabolites of dietary phosphatidylcholine, are known to be associated with cardiovascular disease and with the atherosclerosis process in particular.3,4”
From Bacteroides vulgatus and Bacteroides dorei Reduce Gut Microbial Lipopolysaccharide Production and Inhibit Atherosclerosis (2018) · cites this paper as [3]
In the citing paper
“in the OCA trial for NASH, additional metabolic derangements such as increased blood lipid levels were also observed, in contrast to the findings of other proof of concept studies152,153.”
From Dietary metabolism, the gut microbiome, and heart failure (2019) · cites this paper as [152]
In the citing paper
“Previous studies have shown that the gut microbiota metabolizes choline, phosphatidylcholine, and l-carnitine to produce trimethylamine (TMA), which is oxidized in the liver into the proatherogenic metabolite, trimethylamine-N-oxide (TMAO)11–13.”
From The gut microbiome in atherosclerotic cardiovascular disease (2017) · cites this paper as [11]
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Citations
Cites
A SIMPLE METHOD FOR THE ISOLATION AND PURIFICATION OF TOTAL LIPIDES FROM ANIMAL TISSUES
Folch, J., Lees, M., & Stanley, G. H. S. (1957) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)64849-5 · Cited by 65,189
An obesity-associated gut microbiome with increased capacity for energy harvest
Turnbaugh, P. J., Ley, R. E., Mahowald, M. A., Magrini, V., Mardis, E. R., & Gordon, J. I. (2006) · Nature · doi:10.1038/nature05414 · Cited by 12,444
Human gut microbes associated with obesity
Ley, R. E., Turnbaugh, P. J., Klein, S., & Gordon, J. I. (2006) · Nature · doi:10.1038/4441022a · Cited by 8,785
Diversity of the Human Intestinal Microbial Flora
Eckburg, P. B., Bik, E. M., Bernstein, C. N., Purdom, E., Dethlefsen, L., Sargent, M., Gill, S. R., Nelson, K. E., & Relman, D. A. (2005) · Science · doi:10.1126/science.1110591 · Cited by 7,913
Host-Bacterial Mutualism in the Human Intestine
Bäckhed, F., Ley, R. E., Sonnenburg, J. L., Peterson, D. A., & Gordon, J. I. (2005) · Science · doi:10.1126/science.1104816 · Cited by 5,277
Recognition of Commensal Microflora by Toll-Like Receptors Is Required for Intestinal Homeostasis
Rakoff-Nahoum, S., Paglino, J., Eslami-Varzaneh, F., Edberg, S., & Medzhitov, R. (2004) · Cell · doi:10.1016/j.cell.2004.07.002 · Cited by 4,251
Saikku, P., Mattila, K. J., Nieminen, M. S., Huttunen, J. K., Leinonen, M., Ekman, M.-R., Mäkelä, P. H., & Valtonen, V. (1988) · The Lancet · doi:10.1016/s0140-6736(88)90741-6 · Cited by 1,961
Chronic infections and coronary heart disease: is there a link?
Danesh, J., Collins, R., & Peto, R. (1997) · The Lancet · doi:10.1016/s0140-6736(97)03079-1 · Cited by 1,333
Symbiotic gut microbes modulate human metabolic phenotypes
Li, M., Wang, B., Zhang, M., Rantalainen, M., Wang, S., Zhou, H., Zhang, Y., Shen, J., Pang, X., Zhang, M., et al. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0712038105 · Cited by 1,144
Kunjathoor, V., Febbraio, M., Podrez, E., Moore, K., Andersson, L., Koehn, S. L., Rhee, J. S., Silverstein, R., Hoff, H., & Freeman, M. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m209649200 · Cited by 1,064
Flagged first, then by citations
Research works printed but not linked: 6
- O’Connor, C. M. et al. Azithromycin for the secondary prevention of coronary heart disease events—the WIZARD study: a randomized controlled trial. J. Am. Med. Assoc. 290, 1459–1466 (2003) · DOI
- Andraws, R., Berger, J. S. & Brown, D. L. Effects of antibiotic therapy on outcomes of patients with coronary artery disease: a meta-analysis of randomized controlled trials. J. Am. Med. Assoc. 293, 2641–2647 (2005) · DOI · Paper page
- Wang, S. S. et al. Identification of pathways for atherosclerosis in mice: integration of quantitative trait locus analysis and global gene expression data. Circ. Res. 101, e11–e30 (2007)
- Treberg, J. R., Wilson, C. E., Richards, R. C., Ewart, K. V. & Driedzic, W. R. The freeze-avoidance response of smelt Osmerus mordax: initiation and subsequent suppression of glycerol, trimethylamine oxide and urea accumulation. J. Exp. Biol. 205, 1419–1427 (2002) · DOI · Paper page
- Rizzo, M. L. Statistical Computing with R (Chapman & Hall/CRC, 2008)
- Chen, F. C. M. & Benoiton, L. N. A new method of quatenizing amines and its use in amino acid and peptide chemistry. Can. J. Chem. 54, 3310–3311 (1976) · DOI
Cited by
Sorted by citations
Items 101–200 of 323
The TMAO-Generating Enzyme Flavin Monooxygenase 3 Is a Central Regulator of Cholesterol Balance
Warrier, M., Shih, D. M., Burrows, A. C., Ferguson, D., Gromovsky, A. D., Brown, A. L., Marshall, S., McDaniel, A., Schugar, R. C., Wang, Z., et al. (2015) · Cell Reports · doi:10.1016/j.celrep.2014.12.036 · Cited by 414
Self-citationThe progress of gut microbiome research related to brain disorders
Zhu, S., Jiang, Y., Xu, K., Cui, M., Ye, W., Zhao, G., Jin, L., & Chen, X. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-1705-z · Cited by 419
Role of the gut microbiota in type 2 diabetes and related diseases
Yang, G., Wei, J., Liu, P., Zhang, Q., Tian, Y., Hou, G., Meng, L., Xin, Y., & Jiang, X. (2021) · Metabolism · doi:10.1016/j.metabol.2021.154712 · Cited by 418
Fecal Microbiota Transplantation in Neurological Disorders
Vendrik, K. E. W., Ooijevaar, R. E., de Jong, P. R. C., Laman, J. D., van Oosten, B. W., van Hilten, J. J., Ducarmon, Q. R., Keller, J. J., Kuijper, E. J., & Contarino, M. F. (2020) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2020.00098 · Cited by 413
Wang, H., Rong, X., Zhao, G., Zhou, Y., Xiao, Y., Ma, D., Jin, X., Wu, Y., Yan, Y., Yang, H., et al. (2022) · Cell Metabolism · doi:10.1016/j.cmet.2022.02.010 · Cited by 411
Self-citationLee, G., You, H. J., Bajaj, J. S., Joo, S. K., Yu, J., Park, S., Kang, H., Park, J. H., Kim, J. H., Lee, D. H., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-18754-5 · Cited by 395
The blood exposome and its role in discovering causes of disease
Rappaport, S. M., Barupal, D. K., Wishart, D., Vineis, P., & Scalbert, A. (2014) · Environmental Health Perspectives · doi:10.1289/ehp.1308015 · Cited by 393
Role of the Gut Microbiome in Uremia: A Potential Therapeutic Target
Ramezani, A., Massy, Z. A., Meijers, B., Evenepoel, P., Vanholder, R., & Raj, D. S. (2016) · American Journal of Kidney Diseases · doi:10.1053/j.ajkd.2015.09.027 · Cited by 394
The gut microbiota modulates host amino acid and glutathione metabolism in mice
Mardinoglu, A., Shoaie, S., Bergentall, M., Ghaffari, P., Zhang, C., Larsson, E., Bäckhed, F., & Nielsen, J. (2015) · Molecular Systems Biology · doi:10.15252/msb.20156487 · Cited by 383
Organ, C. L., Otsuka, H., Bhushan, S., Wang, Z., Bradley, J., Trivedi, R., Polhemus, D. J., Tang, W. H. W., Wu, Y., Hazen, S. L., et al. (2016) · Circulation: Heart Failure · doi:10.1161/circheartfailure.115.002314 · Cited by 382
Self-citationGenetic and environmental control of host-gut microbiota interactions
Org, E., Parks, B. W., Joo, J. W. J., Emert, B., Schwartzman, W., Kang, E. Y., Mehrabian, M., Pan, C., Knight, R., Gunsalus, R., et al. (2015) · Genome Research · doi:10.1101/gr.194118.115 · Cited by 381
Self-citationRETRACTED ARTICLE: Role of the gut microbiome in chronic diseases: a narrative review
Vijay, A., & Valdes, A. M. (2022) · European Journal of Clinical Nutrition · doi:10.1038/s41430-021-00991-6 · Cited by 361
RetractedGoldberg, B., Sichtig, H., Geyer, C., Ledeboer, N., & Weinstock, G. M. (2015) · mBio · doi:10.1128/mbio.01888-15 · Cited by 360
Gut Microbiota Promote Angiotensin II–Induced Arterial Hypertension and Vascular Dysfunction
Karbach, S. H., Schönfelder, T., Brandão, I., Wilms, E., Hörmann, N., Jäckel, S., Schüler, R., Finger, S., Knorr, M., Lagrange, J., et al. (2016) · Journal of the American Heart Association · doi:10.1161/jaha.116.003698 · Cited by 378
Breast cancer in postmenopausal women is associated with an altered gut metagenome
Zhu, J., Liao, M., Yao, Z., Liang, W., Li, Q., Liu, J., Yang, H., Ji, Y., Wei, W., Tan, A., et al. (2018) · Microbiome · doi:10.1186/s40168-018-0515-3 · Cited by 377
A novel SCFA receptor, the microbiota, and blood pressure regulation
Pluznick, J. (2014) · Gut Microbes · doi:10.4161/gmic.27492 · Cited by 374
Carnitine metabolism to trimethylamine by an unusual Rieske-type oxygenase from human microbiota
Zhu, Y., Jameson, E., Crosatti, M., Schäfer, H., Rajakumar, K., Bugg, T. D. H., & Chen, Y. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1316569111 · Cited by 372
A healthy gastrointestinal microbiome is dependent on dietary diversity
Heiman, M. L., & Greenway, F. L. (2016) · Molecular Metabolism · doi:10.1016/j.molmet.2016.02.005 · Cited by 370
Flavin-containing monooxygenase 3 as a potential player in diabetes-associated atherosclerosis
Miao, J., Ling, A. V., Manthena, P. V., Gearing, M. E., Graham, M. J., Crooke, R. M., Croce, K. J., Esquejo, R. M., Clish, C. B., Morbid Obesity Study Group, et al. (2015) · Nature Communications · doi:10.1038/ncomms7498 · Cited by 368
Wu, K., Yuan, Y., Yu, H., Dai, X., Wang, S., Sun, Z., Wang, F., Fei, H., Lin, Q., Jiang, H., et al. (2020) · Blood · doi:10.1182/blood.2019003990 · Cited by 345
Fennema, D., Phillips, I. R., & Shephard, E. A. (2016) · Drug Metabolism and Disposition · doi:10.1124/dmd.116.070615 · Cited by 355
Chu, H., Duan, Y., Yang, L., & Schnabl, B. (2019) · Gut · doi:10.1136/gutjnl-2018-316307 · Cited by 354
Dietary trimethylamine N-oxide exacerbates impaired glucose tolerance in mice fed a high fat diet
Gao, X., Liu, X., Xu, J., Xue, C., Xue, Y., & Wang, Y. (2014) · Journal of Bioscience and Bioengineering · doi:10.1016/j.jbiosc.2014.03.001 · Cited by 360
The influence of non-steroidal anti-inflammatory drugs on the gut microbiome
Rogers, M. A. M., & Aronoff, D. M. (2016) · Clinical Microbiology and Infection · doi:10.1016/j.cmi.2015.10.003 · Cited by 346
Association between polycystic ovary syndrome and gut microbiota
Guo, Y., Qi, Y., Yang, X., Zhao, L., Wen, S., Liu, Y., & Tang, L. (2016) · PLOS ONE · doi:10.1371/journal.pone.0153196 · Cited by 350
Taurocholic acid metabolism by gut microbes and colon cancer
Ridlon, J. M., Wolf, P. G., & Gaskins, H. R. (2016) · Gut Microbes · doi:10.1080/19490976.2016.1150414 · Cited by 327
Loss of Gut Microbiota Alters Immune System Composition and Cripples Postinfarction Cardiac Repair
Tang, T. W. H., Chen, H.-C., Chen, C.-Y., Yen, C. Y. T., Lin, C.-J., Prajnamitra, R. P., Chen, L.-L., Ruan, S.-C., Lin, J.-H., Lin, P.-J., et al. (2019) · Circulation · doi:10.1161/circulationaha.118.035235 · Cited by 348
Microbial Metabolite Signaling Is Required for Systemic Iron Homeostasis
Das, N. K., Schwartz, A. J., Barthel, G., Inohara, N., Liu, Q., Sankar, A., Hill, D. R., Ma, X., Lamberg, O., Schnizlein, M. K., et al. (2020) · Cell Metabolism · doi:10.1016/j.cmet.2019.10.005 · Cited by 331
Missailidis, C., Hällqvist, J., Qureshi, A. R., Barany, P., Heimbürger, O., Lindholm, B., Stenvinkel, P., & Bergman, P. (2016) · PLOS ONE · doi:10.1371/journal.pone.0141738 · Cited by 338
Tang, W. H. W., Wang, Z., Shrestha, K., Borowski, A. G., Wu, Y., Troughton, R. W., Klein, A. L., & Hazen, S. L. (2015) · Journal of Cardiac Failure · doi:10.1016/j.cardfail.2014.11.006 · Cited by 325
Self-citationShih, D. M., Wang, Z., Lee, R., Meng, Y., Che, N., Charugundla, S., Qi, H., Wu, J., Pan, C., Brown, J. M., et al. (2015) · Journal of Lipid Research · doi:10.1194/jlr.m051680 · Cited by 335
Self-citationWang, Z., Levison, B. S., Hazen, J. E., Donahue, L., Li, X.-M., & Hazen, S. L. (2014) · Analytical Biochemistry · doi:10.1016/j.ab.2014.03.016 · Cited by 320
Self-citationMirji, G., Worth, A., Bhat, S. A., El Sayed, M., Kannan, T., Goldman, A. R., Tang, H.-Y., Liu, Q., Auslander, N., Dang, C. V., et al. (2022) · Science Immunology · doi:10.1126/sciimmunol.abn0704 · Cited by 327
l-Carnitine in omnivorous diets induces an atherogenic gut microbial pathway in humans
Koeth, R. A., Lam-Galvez, B. R., Kirsop, J., Wang, Z., Levison, B. S., Gu, X., Copeland, M. F., Bartlett, D., Cody, D. B., Dai, H. J., et al. (2018) · Journal of Clinical Investigation · doi:10.1172/jci94601 · Cited by 327
Self-citationThe Role of the Immune System in Metabolic Health and Disease
Zmora, N., Bashiardes, S., Levy, M., & Elinav, E. (2017) · Cell Metabolism · doi:10.1016/j.cmet.2017.02.006 · Cited by 323
Gut reactions: Breaking down xenobiotic–microbiome interactions
Clarke, G., Sandhu, K. V., Griffin, B. T., Dinan, T. G., Cryan, J. F., & Hyland, N. P. (2019) · Pharmacological Reviews · doi:10.1124/pr.118.015768 · Cited by 319
The gut microbiota regulates white adipose tissue inflammation and obesity via a family of microRNAs
Virtue, A. T., McCright, S. J., Wright, J. M., Jimenez, M. T., Mowel, W. K., Kotzin, J. J., Joannas, L., Basavappa, M. G., Spencer, S. P., Clark, M. L., et al. (2019) · Science Translational Medicine · doi:10.1126/scitranslmed.aav1892 · Cited by 317
Emoto, T., Yamashita, T., Sasaki, N., Hirota, Y., Hayashi, T., So, A., Kasahara, K., Yodoi, K., Matsumoto, T., Mizoguchi, T., et al. (2016) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.32672 · Cited by 315
Rapid gut dysbiosis induced by stroke exacerbates brain infarction in turn
Xu, K., Gao, X., Xia, G., Chen, M., Zeng, N., Wang, S., You, C., Tian, X., Di, H., Tang, W., et al. (2021) · Gut · doi:10.1136/gutjnl-2020-323263 · Cited by 308
Self-citationA Combined Epidemiologic and Metabolomic Approach Improves CKD Prediction
Rhee, E. P., Clish, C. B., Ghorbani, A., Larson, M. G., Elmariah, S., McCabe, E., Yang, Q., Cheng, S., Pierce, K., Deik, A., et al. (2013) · Journal of the American Society of Nephrology · doi:10.1681/asn.2012101006 · Cited by 307
Risk of cardiomyopathy and cardiac arrhythmias in patients with nonalcoholic fatty liver disease
Anstee, Q. M., Mantovani, A., Tilg, H., & Targher, G. (2018) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-018-0010-0 · Cited by 310
Transforming berberine into its intestine-absorbable form by the gut microbiota
Feng, R., Shou, J.-W., Zhao, Z.-X., He, C.-Y., Ma, C., Huang, M., Fu, J., Tan, X.-S., Li, X.-Y., Wen, B.-Y., et al. (2015) · Scientific Reports · doi:10.1038/srep12155 · Cited by 307
Guasch-Ferré, M., Satija, A., Blondin, S. A., Janiszewski, M., Emlen, E., O’Connor, L. E., Campbell, W. W., Hu, F. B., Willett, W. C., & Stampfer, M. J. (2019) · Circulation · doi:10.1161/circulationaha.118.035225 · Cited by 304
Paradoxical association of enhanced cholesterol efflux with increased incident cardiovascular risks
Li, X.-M., Tang, W. H. W., Mosior, M. K., Huang, Y., Wu, Y., Matter, W., Gao, V., Schmitt, D., DiDonato, J. A., Fisher, E. A., et al. (2013) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.113.301373 · Cited by 301
Self-citationTrimethylamine-N-Oxide Instigates NLRP3 Inflammasome Activation and Endothelial Dysfunction
Boini, K. M., Hussain, T., Li, P.-L., & Koka, S. S. (2017) · Cellular Physiology and Biochemistry · doi:10.1159/000484623 · Cited by 302
Evenepoel, P., Poesen, R., & Meijers, B. (2017) · Pediatric Nephrology · doi:10.1007/s00467-016-3527-x · Cited by 305
Trimethylamine N-oxide promotes atherosclerosis via CD36-dependent MAPK/JNK pathway
Geng, J., Yang, C., Wang, B., Zhang, X., Hu, T., Gu, Y., & Li, J. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2017.11.016 · Cited by 297
Zhang, X., Li, Y., Yang, P., Liu, X., Lu, L., Chen, Y., Zhong, X., Li, Z., Liu, H., Ou, C., et al. (2020) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.119.313414 · Cited by 291
Schugar, R. C., Shih, D. M., Warrier, M., Helsley, R. N., Burrows, A., Ferguson, D., Brown, A. L., Gromovsky, A. D., Heine, M., Chatterjee, A., et al. (2017) · Cell Reports · doi:10.1016/j.celrep.2017.05.077 · Cited by 291
Self-citationWallace, B. D., Roberts, A. B., Pollet, R. M., Ingle, J. D., Biernat, K. A., Pellock, S. J., Venkatesh, M. K., Guthrie, L., O’Neal, S. K., Robinson, S. J., et al. (2015) · Chemistry & Biology · doi:10.1016/j.chembiol.2015.08.005 · Cited by 285
Food, immunity, and the microbiome
Tilg, H., & Moschen, A. R. (2015) · Gastroenterology · doi:10.1053/j.gastro.2014.12.036 · Cited by 292
Ke, Y., Li, D., Zhao, M., Liu, C., Liu, J., Zeng, A., Shi, X., Cheng, S., Pan, B., Zheng, L., et al. (2018) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.01.007 · Cited by 285
Chen, K., Zheng, X., Feng, M., Li, D., & Zhang, H. (2017) · Frontiers in Physiology · doi:10.3389/fphys.2017.00139 · Cited by 279
Plant Protein and Animal Proteins: Do They Differentially Affect Cardiovascular Disease Risk?
Richter, C. K., Skulas-Ray, A. C., Champagne, C. M., & Kris-Etherton, P. M. (2015) · Advances in Nutrition · doi:10.3945/an.115.009654 · Cited by 279
Incorporation of therapeutically modified bacteria into gut microbiota inhibits obesity
Chen, Z., Guo, L., Zhang, Y., L. Walzem, R., Pendergast, J. S., Printz, R. L., Morris, L. C., Matafonova, E., Stien, X., Kang, L., et al. (2014) · Journal of Clinical Investigation · doi:10.1172/jci72517 · Cited by 277
International Society of Sports Nutrition Position Stand: Probiotics
Jäger, R., Mohr, A. E., Carpenter, K. C., Kerksick, C. M., Purpura, M., Moussa, A., Townsend, J. R., Lamprecht, M., West, N. P., Black, K., et al. (2019) · Journal of the International Society of Sports Nutrition · doi:10.1186/s12970-019-0329-0 · Cited by 277
Gut Microbe-Generated Trimethylamine N -Oxide From Dietary Choline Is Prothrombotic in Subjects
Zhu, W., Wang, Z., Tang, W. H. W., & Hazen, S. L. (2017) · Circulation · doi:10.1161/circulationaha.116.025338 · Cited by 274
Self-citationMa, G., Pan, B., Chen, Y., Guo, C., Zhao, M., Zheng, L., & Chen, B. (2017) · Bioscience Reports · doi:10.1042/bsr20160244 · Cited by 267
Intersections Between Microbiome and Heart Failure: Revisiting the Gut Hypothesis
Nagatomo, Y., & Tang, W. H. W. (2015) · Journal of Cardiac Failure · doi:10.1016/j.cardfail.2015.09.017 · Cited by 259
Self-citationHost-microbial interactions in the metabolism of therapeutic and diet-derived xenobiotics
Carmody, R. N., & Turnbaugh, P. J. (2014) · Journal of Clinical Investigation · doi:10.1172/jci72335 · Cited by 268
Microbial impact on cholesterol and bile acid metabolism: current status and future prospects
Kriaa, A., Bourgin, M., Potiron, A., Mkaouar, H., Jablaoui, A., Gérard, P., Maguin, E., & Rhimi, M. (2019) · Journal of Lipid Research · doi:10.1194/jlr.r088989 · Cited by 264
The Gut Microbiome: A New Frontier in Autism Research
Mulle, J. G., Sharp, W. G., & Cubells, J. F. (2013) · Current Psychiatry Reports · doi:10.1007/s11920-012-0337-0 · Cited by 262
Bae, S., Ulrich, C. M., Neuhouser, M. L., Malysheva, O., Bailey, L. B., Xiao, L., Brown, E. C., Cushing-Haugen, K. L., Zheng, Y., Cheng, T.-Y. D., et al. (2014) · Cancer Research · doi:10.1158/0008-5472.can-14-1835 · Cited by 253
Metabolomics in Diabetes and Diabetic Complications: Insights from Epidemiological Studies
Jin, Q., & Ma, R. C. W. (2021) · Cells · doi:10.3390/cells10112832 · Cited by 252
Rethinking healthy eating in light of the gut microbiome
Armet, A. M., Deehan, E. C., O’Sullivan, A. F., Mota, J. F., Field, C. J., Prado, C. M., Lucey, A. J., & Walter, J. (2022) · Cell Host & Microbe · doi:10.1016/j.chom.2022.04.016 · Cited by 252
Linking the Microbiota, Chronic Disease, and the Immune System
Hand, T. W., Vujkovic-Cvijin, I., Ridaura, V. K., & Belkaid, Y. (2016) · Trends in Endocrinology & Metabolism · doi:10.1016/j.tem.2016.08.003 · Cited by 247
Gut microbiome response to sucralose and its potential role in inducing liver inflammation in mice
Bian, X., Chi, L., Gao, B., Tu, P., Ru, H., & Lu, K. (2017) · Frontiers in Physiology · doi:10.3389/fphys.2017.00487 · Cited by 258
Trimethylamine-N-oxide (TMAO)-induced atherosclerosis is associated with bile acid metabolism
Ding, L., Chang, M., Guo, Y., Zhang, L., Xue, C., Yanagita, T., Zhang, T., & Wang, Y. (2018) · Lipids in Health and Disease · doi:10.1186/s12944-018-0939-6 · Cited by 250
Evolution, human-microbe interactions, and life history plasticity
Rook, G., Bäckhed, F., Levin, B. R., McFall-Ngai, M. J., & McLean, A. R. (2017) · The Lancet · doi:10.1016/s0140-6736(17)30566-4 · Cited by 246
Trimethylamine N-oxide and prognosis in acute heart failure
Suzuki, T., Heaney, L. M., Bhandari, S. S., Jones, D. J. L., & Ng, L. L. (2016) · Heart · doi:10.1136/heartjnl-2015-308826 · Cited by 253
Hou, Y.-F., Shan, C., Zhuang, S.-Y., Zhuang, Q.-Q., Ghosh, A., Zhu, K.-C., Kong, X.-K., Wang, S.-M., Gong, Y.-L., Yang, Y.-Y., et al. (2021) · Microbiome · doi:10.1186/s40168-020-00988-6 · Cited by 231
Miller, C. A., Corbin, K. D., da Costa, K.-A., Zhang, S., Zhao, X., Galanko, J. A., Blevins, T., Bennett, B. J., O’Connor, A., & Zeisel, S. H. (2014) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.114.087692 · Cited by 240
Self-citationAssociation Between Plant and Animal Protein Intake and Overall and Cause-Specific Mortality
Huang, J., Liao, L. M., Weinstein, S. J., Sinha, R., Graubard, B. I., & Albanes, D. (2020) · JAMA Internal Medicine · doi:10.1001/jamainternmed.2020.2790 · Cited by 243
Non-alcoholic fatty liver and the gut microbiota
Bashiardes, S., Shapiro, H., Rozin, S., Shibolet, O., & Elinav, E. (2016) · Molecular Metabolism · doi:10.1016/j.molmet.2016.06.003 · Cited by 241
Joyce, S. A., & Gahan, C. G. M. (2016) · Annual Review of Food Science and Technology · doi:10.1146/annurev-food-041715-033159 · Cited by 241
Fecal microbiota transplantation broadening its application beyond intestinal disorders
Xu, M.-Q. (2015) · World Journal of Gastroenterology · doi:10.3748/wjg.v21.i1.102 · Cited by 231
Metabolic Perturbance in Autism Spectrum Disorders: A Metabolomics Study
Ming, X., Stein, T. P., Barnes, V., Rhodes, N., & Guo, L. (2012) · Journal of Proteome Research · doi:10.1021/pr300910n · Cited by 234
Diet, genetics, and the gut microbiome drive dynamic changes in plasma metabolites
Fujisaka, S., Avila-Pacheco, J., Soto, M., Kostic, A., Dreyfuss, J. M., Pan, H., Ussar, S., Altindis, E., Li, N., Bry, L., et al. (2018) · Cell Reports · doi:10.1016/j.celrep.2018.02.060 · Cited by 231
“…the plasma levels of trimethylamine-N-oxide, another bacterial metabolite that has been linked to cardiovascular disease risk (Tang et al., 2013; Wang et al., 2011b), were markedly decreased by vancomycin, but not metronidazole, in B6J and 129J mice, whereas cecal levels showed no consistent…”
BackgroundCronin, O., Barton, W., Skuse, P., Penney, N. C., Garcia-Perez, I., Murphy, E. F., Woods, T., Nugent, H., Fanning, A., Melgar, S., et al. (2018) · mSystems · doi:10.1128/msystems.00044-18 · Cited by 232
Metabolomics and Cardiovascular Biomarker Discovery
Rhee, E. P., & Gerszten, R. E. (2012) · Clinical Chemistry · doi:10.1373/clinchem.2011.169573 · Cited by 232
Diabetes is Associated with Higher Trimethylamine N-oxide Plasma Levels
Dambrova, M., Latkovskis, G., Kuka, J., Strele, I., Konrade, I., Grinberga, S., Hartmane, D., Pugovics, O., Erglis, A., & Liepinsh, E. (2016) · Experimental and Clinical Endocrinology & Diabetes · doi:10.1055/s-0035-1569330 · Cited by 229
Metabolic Syndrome and PCOS: Pathogenesis and the Role of Metabolites
Chen, W., & Pang, Y. (2021) · Metabolites · doi:10.3390/metabo11120869 · Cited by 228
Lever, M., George, P. M., Slow, S., Bellamy, D., Young, J. M., Ho, M., McEntyre, C. J., Elmslie, J. L., Atkinson, W., Molyneux, S. L., et al. (2014) · PLoS ONE · doi:10.1371/journal.pone.0114969 · Cited by 223
Metabolic, Epigenetic, and Transgenerational Effects of Gut Bacterial Choline Consumption
Romano, K. A., Martinez-del Campo, A., Kasahara, K., Chittim, C. L., Vivas, E. I., Amador-Noguez, D., Balskus, E. P., & Rey, F. E. (2017) · Cell Host & Microbe · doi:10.1016/j.chom.2017.07.021 · Cited by 224
Martínez-del Campo, A., Bodea, S., Hamer, H. A., Marks, J. A., Haiser, H. J., Turnbaugh, P. J., & Balskus, E. P. (2015) · mBio · doi:10.1128/mbio.00042-15 · Cited by 224
Saji, N., Niida, S., Murotani, K., Hisada, T., Tsuduki, T., Sugimoto, T., Kimura, A., Toba, K., & Sakurai, T. (2019) · Scientific Reports · doi:10.1038/s41598-018-38218-7 · Cited by 224
Phages and their potential to modulate the microbiome and immunity
Federici, S., Nobs, S. P., & Elinav, E. (2021) · Cellular & Molecular Immunology · doi:10.1038/s41423-020-00532-4 · Cited by 222
The influence of the gut microbiome on obesity, metabolic syndrome and gastrointestinal disease
Parekh, P. J., Balart, L. A., & Johnson, D. A. (2015) · Clinical and Translational Gastroenterology · doi:10.1038/ctg.2015.16 · Cited by 219
Subchronic Exposure of Mice to Cadmium Perturbs Their Hepatic Energy Metabolism and Gut Microbiome
Zhang, S., Jin, Y., Zeng, Z., Liu, Z., & Fu, Z. (2015) · Chemical Research in Toxicology · doi:10.1021/acs.chemrestox.5b00237 · Cited by 220
Mueller, D. M., Allenspach, M., Othman, A., Saely, C. H., Muendlein, A., Vonbank, A., Drexel, H., & von Eckardstein, A. (2015) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2015.10.091 · Cited by 217
Li, T., Chen, Y., Gua, C., & Li, X. (2017) · Frontiers in Physiology · doi:10.3389/fphys.2017.00350 · Cited by 216
A metabolomic study of biomarkers of meat and fish intake
Cheung, W., Keski-Rahkonen, P., Assi, N., Ferrari, P., Freisling, H., Rinaldi, S., Slimani, N., Zamora-Ros, R., Rundle, M., Frost, G., et al. (2017) · The American Journal of Clinical Nutrition · doi:10.3945/ajcn.116.146639 · Cited by 206
Ufnal, M., Jazwiec, R., Dadlez, M., Drapala, A., Sikora, M., & Skrzypecki, J. (2014) · Canadian Journal of Cardiology · doi:10.1016/j.cjca.2014.09.010 · Cited by 205
Shortt, C., Hasselwander, O., Meynier, A., Nauta, A., Fernández, E. N., Putz, P., Rowland, I., Swann, J., Türk, J., Vermeiren, J., et al. (2018) · European Journal of Nutrition · doi:10.1007/s00394-017-1546-4 · Cited by 194
Xu, R., Wang, Q., & Li, L. (2015) · BMC Genomics · doi:10.1186/1471-2164-16-s7-s4 · Cited by 193
Gong, S., Yan, Z., Liu, Z., Niu, M., Fang, H., Li, N., Huang, C., Li, L., Chen, G., Luo, H., et al. (2019) · Hepatology · doi:10.1002/hep.30361 · Cited by 188
Rohrmann, S., Linseisen, J., Allenspach, M., von Eckardstein, A., & Müller, D. (2016) · The Journal of Nutrition · doi:10.3945/jn.115.220103 · Cited by 197
Enteric Microbiome Metabolites Correlate with Response to Simvastatin Treatment
Kaddurah-Daouk, R., Baillie, R. A., Zhu, H., Zeng, Z.-B., Wiest, M. M., Nguyen, U. T., Wojnoonski, K., Watkins, S. M., Trupp, M., & Krauss, R. M. (2011) · PLoS ONE · doi:10.1371/journal.pone.0025482 · Cited by 193
Skye, S. M., Zhu, W., Romano, K. A., Guo, C.-J., Wang, Z., Jia, X., Kirsop, J., Haag, B., Lang, J. M., DiDonato, J. A., et al. (2018) · Circulation Research · doi:10.1161/circresaha.118.313142 · Cited by 189
Self-citationCollins, H. L., Drazul-Schrader, D., Sulpizio, A. C., Koster, P. D., Williamson, Y., Adelman, S. J., Owen, K., Sanli, T., & Bellamine, A. (2016) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2015.10.108 · Cited by 189
Metadata
- Authors
- Wang, Z., Klipfell, E., Bennett, B. J., Koeth, R., Levison, B. S., DuGar, B., Feldstein, A. E., Britt, E. B., Fu, X., Chung, Y.-M., Wu, Y., Schauer, P., Smith, J. D., Allayee, H., Tang, W. H. W., DiDonato, J. A., Lusis, A. J., & Hazen, S. L.
- Affiliations
- Cleveland Clinic (US)
- University of California, Los Angeles (US)
- Cleveland State University (US)
- University of Southern California (US)
- Corresponding author
- Hazen, Stanley L.
- ORCID
- Venue
- Nature
- Published
- 2011-04
- Volume
- 472
- Issue
- 7341
- Pages
- 57-63
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3086762
- OpenAlex
- W2115944543
- Cited by
- 5,597
- References
- 62
- Citations by year
- 2026: 375 · 2025: 416 · 2024: 451 · 2023: 449 · 2022: 537 · 2021: 563 · 2020: 513 · 2019: 391 · 2018: 380 · 2017: 334 · 2016: 296 · 2015: 266 · 2014: 224 · 2013: 183 · 2012: 157
- FWCI
- 80.19
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- EngagedScholarship @ Cleveland State University (Cleveland State University) (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institute on Alcohol Abuse and Alcoholism (P20AA017837)
- National Heart, Lung, and Blood Institute (P01 HL-30568, P01HL030568, R01HL103931, K99HL102223, P01HL087018-020001, R01HL098193, P01HL076491, P01HL098055, P01-HL28481, P01HL087018, R01HL103866, P01HL028481)
- National Institute of General Medical Sciences (T32GM007250)
- National Institute of Diabetes and Digestive and Kidney Diseases (T32‐DK‐07789, R01DK080732, T32DK007789)
- National Center for Research Resources (UL1RR024989)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolomics and Mass Spectrometry Studies
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- trimethylamine N-oxide, phosphatidylcholine metabolism, gut microbiota, cardiovascular risk, atherosclerosis, choline, betaine, foam cells, macrophage scavenger receptor, flavin-containing monooxygenase, plasma metabolites, germ-free mice, dietary supplementation, cardiovascular risk prediction
- MeSH terms
- Animals, Betaine, Cardiovascular Diseases, Choline, Diet, Dietary Fats, Female, Gene Expression Regulation, Germ-Free Life, Humans, Cholesterol, HDL, Liver, Macrophages, Methylamines, Mice, Inbred C57BL, Oxygenases, Phenotype, Phosphatidylcholines, Biomarkers, Risk Assessment, Gastrointestinal Tract, Atherosclerosis, Receptors, Scavenger, Mice, Metabolomics
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