Major Increase in Microbiota-Dependent Proatherogenic Metabolite TMAO One Year After Bariatric Surgery - PubMed (original) (raw)

Major Increase in Microbiota-Dependent Proatherogenic Metabolite TMAO One Year After Bariatric Surgery

Marius Trøseid et al. Metab Syndr Relat Disord. 2016 May.

Abstract

Background: Trimethylamine-N-oxide (TMAO) is formed in the liver from trimethylamine (TMA), a product exclusively generated by the gut microbiota from dietary phosphatidylcholine and carnitine. An alternative pathway of TMAO formation from carnitine is via the microbiota-dependent intermediate γ-butyrobetaine (γBB). Elevated TMAO levels are associated with cardiovascular disease (CVD), but little is known about TMAO in obesity. Given the proposed contribution of microbiota alterations in obesity and type 2 diabetes (T2D), we investigated the potential impact of obesity, lifestyle-induced weight loss, and bariatric surgery on plasma levels of TMAO, its microbiota-dependent intermediate γBB, and its diet-dependent precursors carnitine and choline.

Methods: TMAO, γBB, carnitine, and choline were measured by high-performance liquid chromatography in 34 obese individuals (17 with and 17 without T2D) undergoing bariatric surgery and 17 controls.

Results: TMAO was not elevated in obese patients or reduced by lifestyle interventions but increased approximately twofold after bariatric surgery. Similar to TMAO, plasma levels of γBB were not influenced by lifestyle interventions but increased moderately after bariatric surgery. In contrast, carnitine and choline, which are abundant in nutrients, such as in red meat and eggs, and not microbiota dependent, were reduced after lifestyle interventions and rebounded after bariatric surgery.

Conclusions: The major increase in TMAO after bariatric surgery was unexpected because high TMAO levels have been linked to CVD, whereas bariatric surgery is known to reduce CVD risk. Prospective studies of gut microbiota composition and related metabolites in relation to long-term cardiovascular risk after bariatric surgery are warranted.

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Figures

<b>FIG. 1.</b>

**FIG. 1.

Plasma levels of choline (A), carnitine (B), trimethylamine-N_-oxide (TMAO) (C), and γ-butyrobetaine (D) in controls (dark gray bars) and morbidly obese subjects (light gray bars) at baseline, after lifestyle intervention (preoperative), and 1 year after surgery (postoperative). Data presented as mean (95% CI). ***P < 0.001, **P < 0.01, versus baseline; †††_P < 0.001, ††P < 0.01, †P < 0.05 versus preoperative.

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References

    1. Pradhan A. Obesity, metabolic syndrome, and type 2 diabetes: Inflammatory basis of glucose metabolic disorders. Nutr Rev 2007;65:S152–S156 - PubMed
    1. Tremaroli V, Backhed F. Functional interactions between the gut microbiota and host metabolism. Nature 2012;489:242–249 - PubMed
    1. Burcelin R, Serino M, Chabo C, et al. Gut microbiota and diabetes: From pathogenesis to therapeutic perspective. Acta Diabetol 2011;48:257–273 - PMC - PubMed
    1. Troseid M, Nestvold TK, Rudi K, et al. Plasma lipopolysaccharide is closely associated with glycemic control and abdominal obesity: Evidence from bariatric surgery. Diabetes Care 2013;36:3627–3632 - PMC - PubMed
    1. Backhed F. Meat-metabolizing bacteria in atherosclerosis. Nat Med 2013;19:533–534 - PubMed

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