Newer Insights into the Taurinuria of Vitamin D Deficiency: A Review - Springer
Excessive taurinuria occurs in vitamin D deficiency as a component of the generalized aminoaciduria of that state. Aminoaciduria was originally ascribed to hyperparathyroidism (increased PTH) in vitamin D-deficiency rickets, especially because aminoaciduria and the increase in PTH disappear after vitamin D repletion. Dabbagh showed that (1) increased taurinuria was due to a defect in the proximal tubule brush border membrane; (2) The Vmax of taurine uptake into brush border membrane vesicles was reduced, possibly related to a paucity of the TauT transporter in the membrane; (3) Animals with low PTH and vitamin D deficiency still had taurinuria and decreased taurine uptake; (4) cAMP incubation did not alter BBMV taurine uptake. The observation that vitamin D-deficiency rickets due to a vitamin D receptor (VDR) mutation results in aminoaciduria despite normal or high 25(OH)D and 1,25(OH)2D values suggests a role for the VDR in taurinuria. Han and Chesney have shown a vitamin D response element (VDRE) in the promoter region of the TauT gene which, under conditions of vitamin D deficiency, results in reduced transcription and reduced TauT protein in LLC-PK1 cells. Thus, in vitamin D deficiency, lower VDRE activation results in lower levels of taurine uptake by tubule cells (or vesicles) and taurinuria. Repletion of 1,25(OH)2D restores TauT transporter activity and taurinuria abates.
Excessive taurinuria occurs in vitamin D deficiency as a component of the generalized aminoaciduria of that state. Aminoaciduria was originally ascribed to hyperparathyroidism (increased PTH) in vitamin D-deficiency rickets, especially because aminoaciduria and the increase in PTH disappear after vitamin D repletion. Dabbagh showed that (1) increased taurinuria was due to a defect in the proximal tubule brush border membrane; (2) The Vmax of taurine uptake into brush border membrane vesicles was reduced, possibly related to a paucity of the TauT transporter in the membrane; (3) Animals with low PTH and vitamin D deficiency still had taurinuria and decreased taurine uptake; (4) cAMP incubation did not alter BBMV taurine uptake. The observation that vitamin D-deficiency rickets due to a vitamin D receptor (VDR) mutation results in aminoaciduria despite normal or high 25(OH)D and 1,25(OH)2D values suggests a role for the VDR in taurinuria. Han and Chesney have shown a vitamin D response element (VDRE) in the promoter region of the TauT gene which, under conditions of vitamin D deficiency, results in reduced transcription and reduced TauT protein in LLC-PK1 cells. Thus, in vitamin D deficiency, lower VDRE activation results in lower levels of taurine uptake by tubule cells (or vesicles) and taurinuria. Repletion of 1,25(OH)2D restores TauT transporter activity and taurinuria abates.