Trimethylamine N-Oxide: The Good, the Bad and the Unknown
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 det...
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Language: | English |
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MDPI AG
2016-11-01
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Series: | Toxins |
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Online Access: | http://www.mdpi.com/2072-6651/8/11/326 |
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author | Manuel T. Velasquez Ali Ramezani Alotaibi Manal Dominic S. Raj |
author_facet | Manuel T. Velasquez Ali Ramezani Alotaibi Manal Dominic S. Raj |
author_sort | Manuel T. Velasquez |
collection | DOAJ |
description | 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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format | Article |
id | doaj.art-15f6b235d3454d6ba73bf045175a66a4 |
institution | Directory Open Access Journal |
issn | 2072-6651 |
language | English |
last_indexed | 2024-04-13T06:44:29Z |
publishDate | 2016-11-01 |
publisher | MDPI AG |
record_format | Article |
series | Toxins |
spelling | doaj.art-15f6b235d3454d6ba73bf045175a66a42022-12-22T02:57:38ZengMDPI AGToxins2072-66512016-11-0181132610.3390/toxins8110326toxins8110326Trimethylamine N-Oxide: The Good, the Bad and the UnknownManuel T. Velasquez0Ali Ramezani1Alotaibi Manal2Dominic S. Raj3Division of Renal Diseases and Hypertension, The George Washington University School of Medicine, 2150 Pennsylvania Avenue NW, Washington, DC 20037, USADivision of Renal Diseases and Hypertension, The George Washington University School of Medicine, 2150 Pennsylvania Avenue NW, Washington, DC 20037, USADivision of Renal Diseases and Hypertension, The George Washington University School of Medicine, 2150 Pennsylvania Avenue NW, Washington, DC 20037, USADivision of Renal Diseases and Hypertension, The George Washington University School of Medicine, 2150 Pennsylvania Avenue NW, Washington, DC 20037, USATrimethylamine 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.http://www.mdpi.com/2072-6651/8/11/326microbiomedysbiosisuremic toxincardiovascular disease |
spellingShingle | Manuel T. Velasquez Ali Ramezani Alotaibi Manal Dominic S. Raj Trimethylamine N-Oxide: The Good, the Bad and the Unknown Toxins microbiome dysbiosis uremic toxin cardiovascular disease |
title | Trimethylamine N-Oxide: The Good, the Bad and the Unknown |
title_full | Trimethylamine N-Oxide: The Good, the Bad and the Unknown |
title_fullStr | Trimethylamine N-Oxide: The Good, the Bad and the Unknown |
title_full_unstemmed | Trimethylamine N-Oxide: The Good, the Bad and the Unknown |
title_short | Trimethylamine N-Oxide: The Good, the Bad and the Unknown |
title_sort | trimethylamine n oxide the good the bad and the unknown |
topic | microbiome dysbiosis uremic toxin cardiovascular disease |
url | http://www.mdpi.com/2072-6651/8/11/326 |
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