Some form of allosteric competition between taurine and GLUT1 may be relevant, but GLUT1 is commonly inhibited by vitamin C rather than by amino acids. Inhibition of the Na +-independent glucose transporter 1 (GLUT1) in activated macrophages (RAW264.7 cells) by taurine chloramine represents one mechanism by which inflammatory cell function can be modulated. While it is tempting to assume that taurine molecules in the tubular lumen compete for sodium and hence reduce glucose uptake, the much higher concentration of glucose (5.0 mM) makes this unlikely. Taurine in the glomerular ultrafiltrate appears to blunt the rate of Na +-dependent uptake of glucose by renal tubules and can potentially lead to glucosuria. Taurine and its transporter also interact with glucose. That taurine egress is dependent on specific ions suggests that it is not purely passive diffusion, but probably involves a carrier-facilitated process. Efflux is much slower than uptake and has a higher K m. It does not contribute to the renal adaptive response described below. Taurine efflux from renal cells is dependent on the intracellular taurine concentration and requires the presence of both Na + and Cl - in the system. In a proximal tubule cell line (LLC-PK1), uptake is maximal on the apical surface in a distal tubule cell line (MDCK), uptake occurs at the basolateral surface (Figure 2). Taurine transport is stereospecific, inhibited by other ß-amino acids and GABA (gamma-aminobutyric acid) but not by α-amino acids, and is membrane surface-specific. ![]() Sodium and chloride move into cells by means of an external to internal downhill Na + gradient (a chemical gradient), and then the sodium is pumped out of the cell by Na +K +-dependent ATPase. The model that best describes this transport is 2 Na +:1 taurine:1 Cl - (Figure 1). In addition to sodium, taurine uptake by renal epithelia requires chloride or bromide. The active uphill transport of taurine occurs via a sodium-dependent transporter (TauT). Some of these properties lead to the role of conjugation of bile acids and uridine in tRNA. It has the lowest pK 1 and pK 2 of all amino acids. Its accumulation within the cell requires active transport from the extracellular environment, where it is found in only micromolar quantities. The taurine molecule acts as a zwitterion at physiologic pH and resides within the cell in millimolar quantities. ![]() Taurine is not incorporated into protein, and can serve as an intracellular osmolyte. It is readily soluble in aqueous solutions. The physiochemical properties of the ß-amino acid taurine are probably responsible for some of its biologic characteristics. In addition, the role of taurine in the pathophysiology of kidney disease will be examined. Thus, this review will focus on several aspects of renal function in relation to taurine and will cover large biologic themes. The numerous physiologic regulators of taurine handling by the kidney have been recently reviewed. ![]() Taurine participates in several biologic processes in the kidney, and the kidney influences specific aspects of taurine homeostasis. The interactions between the kidney and taurine are many and varied.
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