Team:UFMG Brazil/Cardbio
From 2013.igem.org
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Trimethylamine N-oxide (TMAO) is a relatively common diet metabolite in animals. It originates from the degradation of choline, present in the phosphatidylcholine (lecithin) from food like eggs, milk, liver, red meat, poultry, shellfish and fish. Choline and other trimethylamine-containing species (for example, betaine) are degraded by intestinal microbes, forming the gas trimethylamine (TMA). This molecule is then absorbed and metabolized in the liver by flavin monooxygenases (FMO), forming TMAO (Wang et al., 2011). | Trimethylamine N-oxide (TMAO) is a relatively common diet metabolite in animals. It originates from the degradation of choline, present in the phosphatidylcholine (lecithin) from food like eggs, milk, liver, red meat, poultry, shellfish and fish. Choline and other trimethylamine-containing species (for example, betaine) are degraded by intestinal microbes, forming the gas trimethylamine (TMA). This molecule is then absorbed and metabolized in the liver by flavin monooxygenases (FMO), forming TMAO (Wang et al., 2011). | ||
- | A study published in 2013 (Tang et al., 2013) associated TMAO levels in blood with heart disease, and that gut flora has an important role in forming this molecule in humans. The demonstrated relationship between TMAO levels and future cardiac events like heart attack, stroke, and death could be established even in cases with no prior evidence of cardiac disease shown by the traditional methods. | + | A study published in 2013 (Tang et al., 2013) associated TMAO levels in blood with heart disease, and pointed that gut flora has an important role in forming this molecule in humans. The demonstrated relationship between TMAO levels and future cardiac events like heart attack, stroke, and death could be established even in cases with no prior evidence of cardiac disease shown by the traditional methods. |
TMAO also alters cholesterol deposition and removal from endothelial cells. Dietary TMAO aggravate the development of atherosclerotic lesions in apolipoprotein E null (apoE−/−) mice without significant alterations in plasma cholesterol, triglycerides, lipoproteins, glucose levels, and hepatic triglyceride content. But the precise molecular mechanisms in which TMAO mediates its proatherosclerotic effect are currently unknown (Koeth et al., 2013). Given this evidence, TMAO could act as good biomarker for prognosis of cardiovascular risk, although more studies are still needed to validate TMAO testing as clinical tool for preventing cardiovascular disease. | TMAO also alters cholesterol deposition and removal from endothelial cells. Dietary TMAO aggravate the development of atherosclerotic lesions in apolipoprotein E null (apoE−/−) mice without significant alterations in plasma cholesterol, triglycerides, lipoproteins, glucose levels, and hepatic triglyceride content. But the precise molecular mechanisms in which TMAO mediates its proatherosclerotic effect are currently unknown (Koeth et al., 2013). Given this evidence, TMAO could act as good biomarker for prognosis of cardiovascular risk, although more studies are still needed to validate TMAO testing as clinical tool for preventing cardiovascular disease. |
Revision as of 00:51, 28 September 2013