Plasma Concentrations of Trimethylamine-N-oxide Are Directly Associated with Dairy Food Consumption and Low-Grade Inflammation in a German Adult Population

Rohrmann, Sabine; Linseisen, Jakob; Allenspach, Martina; Eckardstein, Arnold von; Müller, Daniel

doi:10.3945/jn.115.220103

Cited by 157 publications

(149 citation statements)

References 44 publications

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“…To our knowledge no other studies have investigated hsCRP and TMAO in HIV infection or T2D. Our finding is consistent with recent studies in healthy individuals [44, 45]. Albeit, an association between TMAO and TNF-α has been found [45].…”

Section: Discussionsupporting

confidence: 93%

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HIV-infected persons with type 2 diabetes show evidence of endothelial dysfunction and increased inflammation

et al. 2017

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BackgroundIncreased incidence of cardiovascular diseases (CVD) in both HIV infection and type 2 diabetes (T2D) compared to the general population has been described. Little is known about the combined effect of HIV infection and T2D on inflammation and endothelial function, both of which may contribute to elevated risk of CVD.MethodsCross-sectional study including 50 HIV-infected persons on combination anti-retroviral therapy (cART), with HIV RNA <200 copies/mL (n = 25 with T2D (HIV + T2D+), n = 25 without T2D (HIV + T2D-)) and 50 uninfected persons (n = 22 with T2D (HIV-T2D+) and n = 28 without T2D (HIV-T2D-)). Groups were matched on age and sex.High sensitive C-reactive protein (hsCRP) was used to determine inflammation (cut-off 3 mg/L). The marker of endothelial dysfunction asymmetric dimethylarginine (ADMA) was measured using high performance liquid chromatography. Trimethylamine-N-oxide (TMAO), a microbiota-dependent, pro-atherogenic marker was measured using stable isotope dilution LC/MS/MS.ResultsThe percentage of HIV + T2D+, HIV + T2D-, HIV-T2D+, and HIV-T2D- with hsCRP above cut-off was 50%, 19%, 47%, and 11%, respectively. HIV + T2D+ had elevated ADMA (0.67 μM (0.63-0.72) compared to HIV + T2D- (0.60 μM (0.57-0.64) p = 0.017), HIV-T2D+ (0.57 μM (0.51-63) p = 0.008), and HIV-T2D- (0.55 μM (0.52-0.58) p < 0.001). No differences in TMAO between groups were found. However, a positive correlation between ADMA and TMAO was found in the total population (rs = 0.32, p = 0.001), which was mainly driven by a close correlation in HIV + T2D+ (rs = 0.63, p = 0.001).ConclusionElevated inflammation and evidence of endothelial dysfunction was found in HIV-infected persons with T2D. The effect on inflammation was mainly driven by T2D, while both HIV infection and T2D may contribute to endothelial dysfunction. Whether gut microbiota is a contributing factor to this remains to be determined.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-017-2334-8) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 93%

“…Our finding is consistent with recent studies in healthy individuals [44, 45]. Albeit, an association between TMAO and TNF-α has been found [45]. Hence, the relation between TMAO and inflammation remains unclear.…”

Section: Discussionsupporting

confidence: 92%

HIV-infected persons with type 2 diabetes show evidence of endothelial dysfunction and increased inflammation

et al. 2017

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“…Fasting plasma TMAO concentration in the supplemented group before starting the treatment and for the whole study period in the placebo group was similar to previously reported values in the same age and sex human subjects [23,24]. Since dietary carnitine is metabolized to TMAO in humans [25], L-carnitine supplementation induced tenfold increase in TMAO, observed in the midpoint of the study and maintained elevated until the end of the study.…”

Section: Discussion/conclusionsupporting

confidence: 87%

L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women

et al. 2018

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Background: L-carnitine can be metabolized to trimethylamine N-oxide (TMAO), a molecule that promotes atherogenesis through its interaction with macrophages and lipid metabolism. Objective: The aim of the present study was to assess whether L-carnitine supplementation may promote changes in selected serum biomarkers of atherosclerosis. Methods: Before the start, in the mid-point and after completing the 24-weeks supplementation protocol, fasting blood samples were taken from the antecubital vein. Plasma free L-carnitine and TMAO were determined by the UPLC/MS/MS method. Serum proteins were determined by the enzyme immunoassay method using commercially available kits. Total cholesterol, high-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, and triglycerides have been determined using standard automatic analyzer. Results: L-carnitine supplementation elevated fasting plasma carnitine in the mid-point of our study and it remained increased until the end of supplementation period. Moreover, it induced tenfold increase in plasma TMAO concentration but did not affect serum C-reactive protein, interleukin-6, tumour necrosis factor-α, L-selectin, P-selectin, vascular cell adhesion molecule-1, intercellular adhesion molecule-1 or lipid profile markers. Conclusion: We demonstrated that although oral L-carnitine supplementation significantly increased plasma TMAO concentration, no lipid profile changes or other markers of adverse cardiovascular events were detected in healthy aged women over the period of 24 weeks.

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“…However, not all studies found an association between diet and TMAO levels [22]. In a study involving 271 participants, consumption of meat, egg, or fish was not associated with TMAO, choline, or betaine concentrations [24]. …”

Section: Determinants Of Tmao Levelmentioning

confidence: 99%

Trimethylamine N-Oxide: The Good, the Bad and the Unknown

Velasquez

Ramezani

Manal

et al. 2016

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Trimethylamine N-oxide (TMAO) is a small colorless amine oxide generated from choline, betaine, and carnitine by gut microbial metabolism. It accumulates in the tissue of marine animals in high concentrations and protects against the protein-destabilizing effects of urea. Plasma level of TMAO is determined by a number of factors including diet, gut microbial flora and liver flavin monooxygenase activity. In humans, a positive correlation between elevated plasma levels of TMAO and an increased risk for major adverse cardiovascular events and death is reported. The atherogenic effect of TMAO is attributed to alterations in cholesterol and bile acid metabolism, activation of inflammatory pathways and promotion foam cell formation. TMAO levels increase with decreasing levels of kidney function and is associated with mortality in patients with chronic kidney disease. A number of therapeutic strategies are being explored to reduce TMAO levels, including use of oral broad spectrum antibiotics, promoting the growth of bacteria that utilize TMAO as substrate and the development of target-specific molecules with varying level of success. Despite the accumulating evidence, it is questioned whether TMAO is the mediator of a bystander in the disease process. Thus, it is important to undertake studies examining the cellular signaling in physiology and pathological states in order to establish the role of TMAO in health and disease in humans.

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Plasma Concentrations of Trimethylamine-N-oxide Are Directly Associated with Dairy Food Consumption and Low-Grade Inflammation in a German Adult Population

Cited by 157 publications

References 44 publications

HIV-infected persons with type 2 diabetes show evidence of endothelial dysfunction and increased inflammation

HIV-infected persons with type 2 diabetes show evidence of endothelial dysfunction and increased inflammation

L-Carnitine Supplementation Increases Trimethylamine-N-Oxide but not Markers of Atherosclerosis in Healthy Aged Women

Trimethylamine N-Oxide: The Good, the Bad and the Unknown

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