Novel findings in metabolomics in the PREDIMED study
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1 Novel findings in metabolomics in the PREDIMED study Miguel A. Martinez-Gonzalez University of Navarra, Dpt. Preventive Medicine Dpt. Nutrition Harvard TH Chan School of P. Health
2 U. Barcelona- Rosa Lamuela Maribel Covas G03/140: (Clinic) RD 06/0045: (Univ. Navarra) CIBERobn: 2013 DOG
3 Ros et al. Adv Nutr. 2014;5:330S-6S
4 30% 30% DO
5 PREDIMED RCT Primary end-point (MI, stroke or CV death) 30% 30% Estruch R, et al. N Engl J Med 2013 DO
6
7 34% 22%n.s.
8
9 Known mechanisms: Inflammation Adiponectin Coagulation Endothelial function Oxidative stress & ox-ldl Improved function of HDL Apolipoproteins Metabolic pathways: Largely unknown Candidates (small molecules): & aromatic AA Acylcarnitines Glutamine : Glutamate ratio Gut flora-related metabolites Urea cycle metabolites Lipid subclasses J Nutr 2016 Mar 9 [Epub ahead of print]
10 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
11 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
12 Mediterranean diet, Metabolites, and Cardiovascular Disease 5R01HL : Jul 15, 2013 Jun 30, 2017 Case-cohort study Baseline metabolites & metabolite 1-y change CVD MeDiet Changes in metabolites CVD Subcohort N=783 Cases N=232 Eligible cohort (N=7,447) Metabolites Intermediate CVD risk factors CVD events (number) Year 0 (Baseline) X X Year 1 Year 2 Year 3 Year 4 Year 5 X X X X X X TIME DOG
13 CVD grant: Specific aims Effects of the interventions on changes in plasma levels of metabolites from baseline to year 1. Whether 1-year change in metabolites mediate the effect of the interventions on CVD from years 2 to 5. Whether baseline metabolite levels modify the effect of the interventions on CVD risk.
14 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
15 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
16 Stroke Adjusted for age, sex, intervention group, BMI, smoking (never, current, former), leisure-time physical activity (METs min/day), and family history of premature coronary heart disease. P for interaction (2 df) between each MedDiet intervention group (EVOO and nuts) (binary, yes/no) and the BCAA score (continuous), with 2 cross-product terms (EVOO BCAA and nuts BCAA).
17 Ruiz-Canela et al. Clin Chem. 2016;62: vs. Control (BCAA score): P =0.101 P=0.729
18 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
19 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
20 J Am Heart Assoc. 2016;5: e ,5 AA as continuous variables (per SD) 2 HR of stroke (95% CI) 1,5 1 0,5 0,56 1,81 0,79 0 Gln:Glu Glutamate Glutamine
21 J Am Heart Assoc. 2016;5: e Among participants with high baseline glutamate, the interventions lowered CVD risk by 37% compared to the control diet; the intervention effects were n.s. when baseline glutamate was low (Pinteract.=0.02). HR for CVD (95%)
22 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
23 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
24 Am J Clin Nutr 2016;103: P values for interaction:
25 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
26 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
27 Circulation. 2017;135:
28 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
29 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
30 Am J Clin Nutr (3 rd review) 1) 202 lipid species and CVD risk 2) a MedDiet intervention (supplemented with EVOO or nuts) vs. control and 1-year changes in these molecules 3) 1-year changes in lipid species and subsequent CVD
31 Direct associations with CVD remaining after correction for multiple testing Three Phosphatidylethanolamines PE(34:2), PE(36:2) and PE(36:1) Three Lysophophatidylethanolamines LPE(16:0), LPE(18:2), and LPE(18:0), Phosphatidylethanolamine plasmalogen PEP(36:3) Phosphatidylserine PS(38:4) Two Ceramides C(16:0) and C(22:0) Three Hydroxy-phosphatidylcholines [M+Na]+ OHPCMA(34:2), OHPCMA(36:4) and OHPC(36:4) Four Diacylglycerols DAG(34:2), DAG(34:1), DAG(36:1), and DAG(36:0) Three Triacylglycerols TAG(50:3), TAG(50:2) and TAG(52:3)
32 Inverse associations with CVD remaining after correction for multiple testing Three Cholesterol esters CE(20:5), CE(20:4) and CE(22:5), Phosphatidylcholine PC(40:10) Phosphatidylcholine plasmalogen PCP(36:5) Triacylglycerol TAG(58:8)
33 Families of lipids weighted by # double bonds & carbon atoms & risk of CVD score= lipid level * # carbon atoms * (# double bonds + 1) HR 95% CI for Q5 vs. Q1 P for trend Lysophosphatidylethanolamines 2.47 ( ).004 Phosphatidylethanolamines 1.60 ( Diacylglycerols 1.58 ( ).010 Cholesterol esters 0.40 (
34 MeDiet+EVOO vs control Weighted linear regression
35 Changes in total lipidome by dietary intervention A positive association between average length of acyl chain and diff. In 1-y changes vs control with MedDiet+EVOO Lipids with longer mean acyl chains exhibited greater increases with MedDiet+EVOO (vs. control) than those with shorter chains Average length of acyl chain # double bonds per acyl chain MedDiet + EVOO vs. control + ns MedDiet + nuts vs. control ns ns
36 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
37 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
38 2 Exposures as continuous variables (per SD) Arginine availability score = arginine/ (citrulline + ornithine). HR of CVD (95% CI) 1 0,84 0,79 0,83 0,5 Arginine Arg:ADMA ratio Arg availability Baseline
39 Emerging TRP-KYN pathway Chronic inflammation cardiometabolic disorders A potential mechanism is the transcriptional induction of indoleamine 2,3-dioxygenase (IDO), ratelimiting enzyme of tryptophan (TRP)-kynurenine (KYN) pathway, by pro-inflammatory cytokines. Activation of IDO shifts TRP metabolism from serotonin synthesis to formation of kynurenines. serotonin depression kynurenines MetS & cardiometabol. conditions by: Apoptotic effects Neurotoxic effects Pro-oxidative effects upregulation of inducible NO synthase, phospholipase A2, arachidonic acid, prostaglandin, 5-lipoxygenase, and leukotriene cascade.
40 KYNURINE RISK SCORE (KRS): Normalized individual metabolites weighted by their b coefficient (from a fully adjusted model with that metabolite alone) Increases in tryptophan after 1 y were associated with a lower risk of composite CVD ( 0.79, ) The weights were: 0.13 for tryptophan for kynurenine for kynurenic acid, 0.20 for 3-hydroxyanthranilic acid for quinolinic acid. A higher KRS was more strongly associated with CVD in the control group than in the 2 intervention groups (P-interaction = 0.003)
41 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
42 Metabolomics CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gutmicrobiota Others MedDiet Footprints Ceramides Targeted lipids PCA Pathways-Networks Non-targeted RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
43 Guasch-Ferre, et al. Gut microbiota related plasma metabolites and risk of cardiovascular disease in the PREDIMED Study (submitted) TMAO, betaine, choline, phosphocholine, alphaglycerophosphocholine, proline, hydroxyproline, and allantoin a) Metabolite score b) Betaine/choline ratio 4,0 3,5 P trend < ,6 1,4 P trend = ,0 1,2 Adjusted HR (95% CI) 2,5 2,0 1,5 1,0 213% Adjusted HR (95% CI) 1,0 0,8 0,6 0,4 43% 0,5 0,2 0,0 Q1 (REF) Q2 Q3 Q4 Cases: Cases: Adjusted for age, sex, body mass index, family history of premature heart disease, smoking, physical activity, hypertension, dyslipidemia, and diabetes, and stratified by intervention group 0,0 Q1 (REF) Q2 Q3 Q4
44 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
45 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
46 Metabolomic footprints MedDiet RCT: MeDiet+EVOO vs. Control: discrimination MeDiet+nuts vs. Control: discrimination 14-item screener assessing adherence Baseline Repeated measurements 1-y Food Frequency questionnaires (0, 1-y) EVOO Nuts
47 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
48 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
49 Dietary interventions, metabolites and risk of T2D NIH/NIDDK-R01DK Sep 1, 2014 Ago 31, 2018 Case-cohort study Baseline metabolites & metabolite 1-y change T2DM MeDiet Changes in metabolites T2DM DOG
50 T2D grant: Specific aims Association baseline metabolites & T2D Whether the interventions modify the effect of baseline metabolites and T2D risk. Whether 1-year change in metabolites mediate the effect of the interventions on CVD from years 2 to 5. Whether 1-year change in metabolites influence insulin resistance from years 2 to 5 in a subsample of 708 participantes free of T2D
51 T2D grant
52 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
53 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
54 Diabetes Care 2016;39:833-46
55 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
56 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
57 Plasma amino-acids, their changes after a Mediterranean diet intervention and risk of type 2 diabetes: The randomized PREDIMED Trial Baseline HR of T2D (95% CI) ,5 3,3 Top vs. bottom quartile 2,8 2,3 1,3 Leu Iso Val Phe Tyr 1,9 Working report 4 HR of T2D (95% CI) 2 1 0,5 1,62 1,22 Scores as continuous variables (per SD) BCAA score AA score Changes in scores (per SD) and subsequent risk of T2D
58 Plasma amino-acids, their changes after a Mediterranean diet intervention and risk of type 2 diabetes: The randomized PREDIMED Trial Working report
59 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
60 CVD ( ) Gln/Glu Carnitines Lipidomics Urea cycle Trp/Kynur. Gut-microbiota Others Ceramides Targeted lipids PCA Pathways-Networks Non-targeted Metabolomics MedDiet Footprints RCT intervention P14 EVOO /Nuts T2D ( ) Syst. Review Pending / Other
61 T2D grant: pending 1. Gut microbiota-related metabolites 2. Acylcarnitines 3. Tryptophan, Kynurenines 4. Urea cycle metabolites 5. Lipidomics, 2-bonds, length 6. Lipids PCA 7. 2-Amino-adipic acid 8. Lactate-glycolysis-gluconeogenesis 9. Purine catabolism 10. Uridine 11. Network-Pathways 12. Glutamine cycling pathway 13. Non-targeted metabolites To be presented tomorrow
62 Thank you! Miguel A. Martinez-Gonzalez University of Navarra, Dpt. Preventive Medicine Dpt. Nutrition Harvard TH Chan School of P. Health
63
64 Gln/Glu mechanisms Gln and Glu are transformed into each other as part of numerous physiological processes. Cycling between Gln and Glu is regulated by the activity of glutamine synthetase and glutaminase, enzymes that have wide tissue distribuion. The proposed mechanisms underlying the beneficial effects of Gln include a wide range of metabolic pathways, such as stimulation of insulin secretion via enhancing release of glucagon-like peptide 1 and improvement in insulin sensitivity. Furthermore, Gln has a regulatory capacity in immune cell modulation and has antiobesity and antidiabetic effects.
65 Acyl-carnitine mechanisms meat eaters tend to have increased concentrations of acylcarnitines and other metabolites Various short- and long-chain acylcarnitines possess a trimethylamine moiety, and consequently, they are likely to be involved in gut microbe dependent pathways that contribute to the formation of trimethylamine and trimethylamine-n-oxide, which may increase risk of atherosclerosis and consequently of CVD acylcarnitine concentrations have been associated with increased risks of insulin resistance and type 2 diabetes
66 Acyl-carnitine mechanisms (2) The accumulation of acylcarnitines may be indicative of inefficient b oxidation and altered mitochondrial metabolism. Acylcarnitines are derived from both fatty acid and amino acid betaoxidation. The main function of L-carnitine is to transport fatty acids from the cytosol to the mitochondrial matrix where beta oxidation takes place; this process results in the esterification of L-carnitine to form acylcarnitine derivatives Advanced age leads to an impaired flux of carnitines through the mitochondrial pathway, thereby reflecting mitochondrial dysfunction. an increased mitochondrial production of reactive oxygen species that enhances vascular inflammation and contributes to alterations in the composition of plaque and to its rupture
67 Ceramide mechanisms precursors of complex sphingolipids aberrant accumulation of ceramides may lead to the activation of several signaling and putative targets that impair normal cellular function, including insulin action excess de novo ceramide biosynthesis is linked to cellular stress stimuli, especially to the exposure to saturated free fatty acids (FFAs) Ceramides have been proposed as an intermediate link between overnutrition and certain underlying abnormalities driving cardiometabolic disease risk, including insulin resistance and low-grade inflammation
68 Ceramide mechanisms (2) Earlier studies using cultured cells and animal models suggested that endogenous ceramides antagonized insulin-stimulated glucose uptake and anabolism by blocking activation of Akt/PKB, a serine/ threonine kinase that is obligate for insulin and growth factor activation of anabolism and cell survival human studies have observed positive correlations between plasma ceramide concentrations and inflammatory makers (eg, interleukin-6 and tumor necrosis factor-α), suggesting a relationship between excess ceramides and inflammation
69 Ceramide mechanisms (3) pharmacological inhibition of ceramide biosynthesis prevents atherogenesis Ceramides and other sphingolipids may contribute to plaque erosion and therefore induce thrombosis. These studies on plaque formation also found that inhibition of ceramide biosynthesis caused a reduction of circulating total cholesterol and LDL
70 Lipidome mechanisms The detrimental effect of saturation in triacylglycerols may be attributable to the higher atherogenic potential of saturated fats cholesterol esters, with longer and more unsaturated acyl chains associated with lower the risk of CVD is consistent with a lower diabetes risk observed by Rhee et al., although the association they observed disappeared after multivariable adjustment J Clin Invest. 2011;121:1402 1
71 Lipidome mechanisms (2) Phosphatidylcholines are membrane lipids that are the most abundant lipids in mammal plasma membranes. If phosphatidylcholines with shorter chains and more highly saturated acyl chains are available, this could confer less fluidity to the cell membranes long-chain fatty acids, with many carbon atoms and many double bonds (i.e. long-chain PUFA), mainly omega-3 PUFAs, are associated with reduced triglyceride levels, reduced myocardial oxygen demands and beneficial changes in endothelial function, together with reduced heart rate (and lower heart rate variability) and decreased blood pressure
72 Lipidome mechanisms (3) SFA with a lower number of carbon atoms (16:0) are known to exert more detrimental effects on lipids and cardiovascular disease than those with a higher number of carbon atoms (18.0) (Zong et al, BMJ 206;355:i5796). Long-chain PUFA are also precursors to bioactive lipid metabolites, including specialized pro-resolving mediators and cytochrome P450 generated monoepoxides (Arnold et al, Pharmacol Rep 2010;62:536; Serhan. Am J Pathol 2010;177:1576) hydroxy-phosphatidylcholines can be formed as adducts under conditions of oxidative stress and/or inflammation and may be components of oxidized LDL, thus increasing the risk of CVD
73 Urea cycle mechanisms The Framingham Offspring cohort reported a significantly lower risk of CVD associated with the arginine/adma ratio A meta-analysis of 22 prospective cohort studies with a mean follow-up time of 7.1 years reported a robust association between ADMA concentrations and higher risk of subsequent CVD events (Willeit et al, J Am Heart Assoc 2015;4:e001833) High ADMA in concert with low NO has been reported to propagate a variety of harmful detrimental processes biologically related to atherosclerosis:free radical generation, smooth cell proliferation, systemic inflammation, and endothelial dysfunction
74 Urea cycle mechanisms (2) Arginine (and only L-arginine) is the required substrate for all isoforms of the enzyme NOS to produce NO NO is acknowledged as a powerful short-life vasodilator with an important defensive role against ischemic disease through endothelial smooth muscle relaxation Inhibition of arginase, a competitive inhibitor of arginine, improves vascular integrity, and protects against ischemia-induced injury
75 TRP/KYN mechanisms Indoleamine 2,3-dioxygenase (IDO), an enzyme catalyzing the rate-limiting step in the kynurenine pathway of tryptophan degradation, is strongly induced by inflammation in several tissues, including the artery wall IFN-gamma plays a central role in the activation of IDO and subsequent degradation of tryptophan however, activation of the kynurenine pathway has also been shown to have anti-inflammatory effects. activation of the tryptophan-kynurenine pathway may be a compensatory mechanism to, rather than a cause of, inflammation and cardiovascular dysfunction.
76 TRP/KYN mechanisms (2) Treatment of human peripheral blood mononuclear cells and monocyte-derived macrophages with IFN-g attenuated the extent of LDL oxidation, and tryptophan degradation in concert with 3-HAA formation was instrumental in this inhibitory effect. 3-HAA has also been independently identified as having antiatherogenic properties by regulating lipid me- tabolism and inflammation. Other experimental studies suggest a beneficial effect of IDO on the vasculature. IDO-deficient mice fed high-fat diets showed marked increases in F4/80 and TNF mrna concentrations, as well as greater hepatic inflammation compared with control mice
77 Gut-microbiota related metabolites
78 Gut-microbiota related metabolites (2) Alterations in the gut microbiome have been previously related to multifactorial diseases such as obesity, T2D and CVD, probably through several mechanisms including modulation of host energy metabolism gut epithelial permeability gut peptide hormone secretion and increasing metabolic endotoxemia and inflammatory status. However, the association between plasma gut microbiota related metabolites, identified using novel high-throughput metabolomics techniques, and the incidence of CVD in a population-based level have only recently been reported.
79 Gut-microbiota related metabolites (3) dietary phosphatidylcholine/choline can be converted by the intestinal microbiota into trimethylamine and subsequently converted into TMAO by hepatic flavin-containing monooxigenases and TMAO has been linked with CVD pathogenesis in vivo and in vitro studies suggestthat choline metabolites may increase the risk of atherosclerosis and coronary heart disease The ability of oral broad-spectrum antibiotics to temporarily suppress the production of TMAO suggests that intestinal microorganisms may play an important role in the production of TMAO from phosphatidylcholine in humans
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