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Normally, the FMO3 enzyme converts fishy-smelling trimethylamine into trimethylamine N-oxide which has no odor. If the enzyme is missing or its activity is reduced because of a mutation in the FMO3 gene, trimethylamine is not broken down and instead builds up in the body. As the compound is released in a person's sweat, urine, and breath, it ...
Trimethylamine is a full agonist of human TAAR5, [13] [14] [15] a trace amine-associated receptor that is expressed in the olfactory epithelium and functions as an olfactory receptor for tertiary amines. [15] [16] One or more additional odorant receptors appear to be involved in trimethylamine olfaction in humans as well. [16]
Trimethylaminuria is a rare defect in the production of the enzyme flavin-containing monooxygenase 3 (FMO3). [19] [20] Those suffering from trimethylaminuria are unable to convert choline-derived trimethylamine into trimethylamine oxide. Trimethylamine then accumulates and is released in the person's sweat, urine, and breath, giving off a ...
In the human body, deamination takes place primarily in the liver; however, it can also occur in the kidney. In situations of excess protein intake, deamination is used to break down amino acids for energy. The amino group is removed from the amino acid and converted to ammonia.
Because many proteases are nonspecific, they are highly regulated in the cell. Without regulation, proteases will destroy many proteins which are essential to physiological processes. One way the body regulates proteases is through protease inhibitors. Protease inhibitors can be other proteins, small peptides, or molecules.
Trimethylamine N-oxide reductase (TOR or TMAO reductase, EC 1.7.2.3) is a microbial enzyme that can reduce trimethylamine N-oxide (TMAO) into trimethylamine (TMA), as part of the electron transport chain. The enzyme has been purified from E. coli and the photosynthetic bacteria Roseobacter denitrificans. [1]
A new study explains how mitochondria act as “reservoirs” to store NAD for cells to use, which could help scientists come up with NAD-boosting therapies to combat aging and age-related diseases.
When in need of glucose the body of a person with a fatty-acid metabolism disorder will still send fats to the liver. The fats are broken down to fatty acids. The fatty acids are then transported to the target cells but are unable to be broken down, resulting in a build-up of fatty acids in the liver and other internal organs.