Startseite Changes to trimethylamine-N-oxide and its precursors in nascent metabolic syndrome
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Changes to trimethylamine-N-oxide and its precursors in nascent metabolic syndrome

  • Daniella Lent-Schochet , Ryan Silva , Matthew McLaughlin , Beverley Huet und Ishwarlal Jialal EMAIL logo
Veröffentlicht/Copyright: 18. April 2018
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Abstract

Background

Metabolic syndrome (MetS), a cardio-metabolic cluster afflicting 35% of American adults, increases cardiovascular disease (CVD) and type-2 diabetes (T2DM) risk. Increased levels of trimethylamine N-oxide (TMAO), a metabolite derived from choline and L-carnitine, correlates with CVD and T2DM. However, the precise role of TMAO and its precursors in MetS remains unclear. We tested the hypothesis that choline, L-carnitine and TMAO in MetS patients without CVD or T2DM would be altered and correlate with inflammatory markers.

Materials and methods

This was an exploratory study of 30 patients with nascent MetS (without CVD or T2DM) and 20 matched controls. MetS was defined by the Adult Treatment Panel III criteria. TMAO and its precursors were evaluated from each patient’s frozen early morning urine samples and quantified using liquid chromatography/mass spectrometry (LC-MS). These amines were correlated with a detailed repertoire of biomarkers of inflammation and adipokines.

Results

L-carnitine was significantly increased (p = 0.0002) compared to controls. There was a trend for a significant increase in TMAO levels (p = 0.08). Choline was not significantly altered in MetS. L-carnitine correlated significantly with soluble tumor necrosis factor 1 (sTNFR1) and leptin, and inversely to adiponectin. TMAO correlated with IL-6, endotoxin and chemerin. Neither choline, nor L-carnitine significantly correlated with TMAO.

Conclusion

L-carnitine is directly correlated with markers of inflammation in nascent MetS. Cellular L-carnitine could be a biomediator or marker of inflammation in the pathogenesis of MetS, and the sequelae of CVD and T2DM.

Acknowledgments

The authors thank the American Diabetes Association.

Author Statement

  1. Research funding: This study was funded in part from a grant from the American Diabetes Association to I. Jialal.

  2. Conflict of interest: The authors have no financial or other conflicts of interest to disclose.

  3. Informed consent: All study participants signed an informed consent form obtained and approved by the Institutional Review Board at University of California Davis.

  4. Ethical approval: The research related to human use complied with all the relevant national regulations and institutional policies and was performed in accordance with the tenets of the Helsinki Declaration and has been approved by the Institutional Review Board at University of California Davis.

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Received: 2018-02-07
Accepted: 2018-03-23
Published Online: 2018-04-18

©2018 Walter de Gruyter GmbH, Berlin/Boston

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