Genetic deletion of the taurine transporter (TauT) in mice reduces taurine concentrations in plasma and tissues, including the brain. Both TauT and GAT-2 are also able to efficiently carry hypotaurine. The blood-brain barrier also expresses the GABA transporter SLC6A13, known as GAT-2, which is capable of carrying taurine across membranes. Taurine uptake or efflux at both luminal and albumen membranes has been proposed to be mediated by SLC6A6 transporter, also called TauT. The passive diffusion of taurine across the blood-brain barrier is negligible. Taurine, as well as hypotaurine, β-alanine, and other β-amino acids, are taken up through the blood–brain barrier into the brain by a high-affinity, low-capacity Na +- and Cl −-dependent transport system. ![]() In most mammals, taurine is mainly synthetized in the liver and then actively transported through the blood-brain barrier into the brain parenchyma. Taurine in the brain results from its transport from the periphery (believed to be the main source) and local de novo synthesis. This is clear evidence advocating for the importance of taurine. Enzymes that synthetize taurine show low activity in cats, dogs, and foxes, which develop pathologies when fed a taurine-deficient diet, namely, cardiomyopathy and myocardial dysfunction, retinal degeneration, neurological abnormalities, weakened immune response, pregnancy and fetal development complications, as well as gastrointestinal problems (see and references therein). In addition, brain taurine is known as an osmoregulator and neuromodulator and is involved in numerous processes, such as the modulation of neuronal excitability, the cerebral control of the cardiorespiratory system, appetite regulation, resistance to hypoxia, osmoregulation, and anti-oxidation. Namely, taurine treatments have been shown to protect tissues and cells against oxidative stress (e.g., ), mitochondrial stress (e.g., ), or inflammation (e.g., ). The neuroprotective effects of taurine have received considerable attention, and there is a plethora of publications showing the ability of exogenously added taurine to prevent toxicity in neurons or astrocytes in vitro, as well as in animal models of neurological disorders (reviewed by Jakaria et al. Taurine supplementation has been suggested to have beneficial effects on a number of disorders, for example, hypertension, congestive heart failure, ischemia–reperfusion myocardial injury, intracerebral hemorrhage, pulmonary fibrosis, obesity-induced low-grade inflammation. Together with glycine, taurine is well known for bile acid amidation, producing bile salts for excretion. Taurine is obtained from the diet or results from de novo synthesis through catabolism of the amino acid cysteine ( Figure 1). Taurine, or 2-aminoethanesulfonic acid, was first isolated from ox bile in 1827, by Friedrich Tiedemann and Leopold Gmelin. ![]() We conclude that further research is needed for understanding taurine homeostasis in metabolic disorders with an impact on brain function. The present article provides an overview of brain taurine homeostasis and reviews the mechanisms by which taurine can afford neuroprotection in individuals with obesity and diabetes. Given the possible cytoprotective actions of taurine, such cerebral accumulation of taurine might constitute a compensatory mechanism that attempts to prevent neurodegeneration. On the other hand, models of insulin-dependent diabetes, insulin resistance, and diet-induced obesity display taurine accumulation in the hippocampus. Models of neurodegenerative disorders show reduced brain taurine concentrations. ![]() Alterations to taurine homeostasis can impact a number of biological processes, such as osmolarity control, calcium homeostasis, and inhibitory neurotransmission, and have been reported in both metabolic and neurodegenerative disorders. Obesity, type 2 diabetes, and their associated comorbidities impact brain metabolism and function and constitute risk factors for cognitive impairment.
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