Mechanisms Regulating the Activity of the Taurine Transporter The Na +/Cl −/taurine stoichiometry of the cloned TauT was 2:1:1, and the transporter was specific for taurine and other β-amino acids with a high affinity for taurine. Then, human TauT was cloned from the human placenta using a similar approach. The cDNAs encoding for the taurine transporter (TauT) were first cloned using sequence similarities to glycine, GABA, or other neurotransmitter transporters from Madin–Darby canine kidney cells and mouse and rat brains. Cloning cDNAs for taurine transporter (TauT) revealed an aspect of the molecular basis for taurine transport with these physiological properties. In addition, taurine efflux is stimulated by hypoosmotic conditions. The taurine transport system is energized by a Na + gradient and requires Cl −, and its activity is inhibited by Ca 2+/diacylglycerol-dependent protein kinase (PKC). The molecular system for taurine transport has been revealed by conducting various physiological analyses. Cloning of a Taurine Transporter and Its Function In this review, I provide a comprehensive overview of the functions of taurine in offspring development, the regulatory mechanisms of taurine transport from mother to offspring, and the outcomes of taurine depletion during development.Ģ.1. Taurine is a molecule that links the mother with the offspring. Notably, in cats, in which taurine deficiency during early development leads to severe morphological developments of the retina and cerebellum, the concentration of taurine in milk is very high (2.87 M), being second to that in gerbil (5.95 M). Taurine has the second highest concentration in breast milk after glutamate in these species. Taurine is a principal constituent of the amino acid pool in the milk in many species, including humans, chimpanzees, baboons, rhesus monkeys, Java monkeys, sheep, and rats. Fetuses and infants depend on the taurine supplied by mothers via the placenta or breast milk. In mammals, adults synthesize taurine in the liver from methionine/cystine, although fetuses and infants have limited ability to synthesize taurine because they have limited levels of γ-cystathionase and cysteine sulfinic acid (CSAD) in livers and brains ( Figure 1). In addition, taurine structurally resembles neurotransmitter γ-aminobutyric acid (GABA) and glycine and interacts with both GABA A and glycine receptors to induce chloride currents in neuronal cells. Taurine (2-aminoethanesulfonic acid) is a sulfur-containing organic acid with various biological functions, including membrane stabilization, cell volume regulation, mitochondrial protein translocation, anti-oxidative activity, and modulation of intracellular calcium levels. Thus, it is essential to understand the nature of mother–offspring bonding during pregnancy and the postpartum period and the factors that affect bonding. In addition, offspring development can be affected by early mother–offspring relationships. Not surprisingly, females form their strongest social bonds with their offspring. Only female mammals have the ability to provide prenatal resources through the placenta and produce milk for postnatal development. The possible functions of taurine as a determinant of gut microbiota and in the context of the Developmental Origins of Health and Disease (DOHaD) hypothesis will also be discussed.Ī significant development in the evolution of mammals is placentation, intrauterine development of the fetus, and extensive care after birth that improves infant survival to a reproductive age. I also refer to the possible environmental factors affecting taurine functions in mother-offspring bonding during perinatal periods. In this review, I will discuss the biological function of taurine during development and the regulatory mechanisms of taurine transport from mother to offspring. Thus, maternally derived taurine during the perinatal period can influence the offspring’s development and even determine health and disease later in life. Various environmental factors, including maternal obesity, preeclampsia, and undernutrition, can affect the efficacy of taurine transfer via either the placenta or breast milk. Many lines of evidence demonstrate that maternally derived taurine is essential for offspring development, shaping various traits in adults. Therefore, they are dependent on taurine given from mothers either via the placenta or via breast milk. Mammalian fetuses and infants have little ability to synthesize taurine. Mammals can obtain taurine from food and synthesize it from sulfur-containing amino acids.
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