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involved in protein synthesis and processing in the G2 phase of the cell cycle.
Interestingly, 293 cells possess the characteristics of both renal and neuronal cells.
TauT /taurine deficiency results in brain and kidney maldevelopment (Han et al.
2000b ; Heller-Stilb et al. 2002 ; Ito et al. 2008 ; Sturman 1986 ) . Therefore, our
findings here further unveil the mechanism of the physiologic function of TauT dur-
ing development.
Theoretically, in humans, taurine deficiency mainly occurs in individuals who have
a TauT deficiency caused by kidney disease and/or kidney injury. The human body has
a limited capacity to synthesize taurine, and the kidney controls the total body pool of
taurine. Therefore, models of TauT deficiency would be an ideal tool for studying the
effects of taurine and/or TauT deficiency on kidney diseases and its implications.
Knockdown of TauT strongly reduced GLUT3 expression in 293 cells, suggesting that
TauT may affect glucose metabolism by influencing the expression of GLUT. Others
have shown that high glucose levels downregulate TauT expression and result in intra-
cellular taurine depletion (Askwith et al. 2009 ). Moreover, the bioavailability of taurine
is severely reduced in diabetic patients; it is 30% lower than in matched control sub-
jects and similar to the level found in taurine-deficient cats (Han et al. 2000b ; Merheb
et al. 2007 ) . Thus, TauT /taurine deficiency secondary to hyperglycemia may predis-
pose to diabetic neuropathy and diabetic nephropathy in diabetic patients.
28.5
Conclusion
In conclusion, the results from this study suggest that TauT plays a role in the devel-
opment of renal cells. Knockdown of TauT impairs kidney development, possibly
through regulation of cell cycle-related genes.
Acknowledgements The authors wish to thank Andrea Patters for insightful comments and sug-
gestions. This work was supported by the Le Bonheur Chair of Excellence in Pediatrics.
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