Taurine differs from other amino acids because a sulfur group replaces the carboxyl group of what would be the nonessential amino acid, β-alanine. It takes part in biochemical reactions and is not fully incorporated into proteins.
In most tissues, it remains a free amino acid. Taurine’s highest concentration is in muscle, platelets, and the central nervous system.
Taurine is mainly obtained via dietary sources (dairy, shellfish, turkey, energy drinks), but can also come from sulfur amino acid metabolism (methionine and cysteine).
It has been proposed that taurine acts as an antioxidant, intracellular osmolyte, membrane stabilizer, and a neurotransmitter.
In the CNS, taurine is second only to glutamate in abundance. Taurine is extensively involved in neurological activities, (calming neural excitability, cerebellar functional maintenance, and motor behavior modulation), through interaction with dopaminergic, adrenergic, serotonergic, and cholinergic receptors, and through glutamate.
In cardiovascular disease, taurine’s benefits are multifactorial. Because taurine’s main physiologic role is in bile acid conjugation in the liver, it has been demonstrated that taurine is capable of reducing plasma LDL, total lipid concentration, and visceral fat in diabetic, obese patients.
Taurine has been shown to be a protector of endothelial structure and function after exposure to inflammatory cells, their mediators, or other chemicals.
Taurine is thought to be involved in cell volume regulation and intracellular free calcium concentration modulation. Because of these effects, experimental evidence shows promise for taurine therapy in preventing cardiac damage during bypass surgery, heart transplantation and myocardial infarction. Moreover, severe taurine extravasation from cardiomyocytes during an ischemia–reperfusion insult may increase ventricular remodeling and heart failure risk.
Recent work has revealed taurine’s action in the retina as a photoreceptor cell promoter. The human fetus has no ability to synthesize taurine. Taurine is found in breast milk, but it is also routinely added to infant formulas. Although taurine is very beneficial, it is often unnecessary to supplement. Dietary intake and sulfur amino metabolism are usually more than adequate to meet the body’s needs. Newborns, patients with restricted diets, or patients with various diseases may be depleted in taurine and can benefit from supplementation.
Low levels of amino acids can be seen with poor dietary intake, GI tract malabsorption, or maldigestion. Because of taurine’s role in the transsulfuration pathway, as outlined above, low levels of taurine may also be due to excessive oxidative stress, lack of precursors, or deficient enzymatic cofactors.
Excessive dietary intake of taurine-rich foods/beverages may result in elevated taurine levels (i.e. energy drinks, dairy, shellfish, and turkey).
Because taurine is part of the transsulfuration pathway, a single nucleotide polymorphism (SNP) in the cystathioninebeta-synthase (CBS) enzyme can elevate taurine, but only in the absence of oxidative stress and presence of adequate glutathione levels.
However, because oxidative stress and inflammation can upregulate transsulfuration in general, taurine may also be elevated in response to those factors. Antioxidants, such as vitamins A and E, as well as plant-based antioxidants, can help to mitigate oxidative damage.
As with all sulfur-containing amino acids, the enzyme sulfite oxidase catabolizes the amino acid into sulfite for excretion. An important cofactor for this enzyme is molybdenum. With that, insufficient molybdenum can contribute to elevated taurine levels.
Because renal excretion of taurine depends on a sodium chloride transporter which is regulated by vitamin B1, irregular renal excretion of taurine can be seen in functional vitamin B1 insuffiencies.
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