With vitamin D deficiency, excessive phosphaturia and aminoaciduria are common, but the pathophysiology of these abnormal losses is uncertain. To better understand the pathophysiologic mechanism of aminoaciduria, we placed weanling rats on various vitamin D-deficient diets for 4-7 weeks. The diets were: 1) very low calcium (0.02% Ca) diet (VLCD); 2) low-Ca (0.5%) diet (LCD); 3) normal-Ca (1.2%), low-phosphate (0.1%) diet (LPD). Another VLCD group received 500 pmoles of 1,25(OH)2D intraperitoneally for 2 days before sacrifice (VLCD-1,25). Urinary excretion and isolated brush border membrane vesicle studies were performed, examining glucose and the amino acid taurine (T).
All * parameters were different from control at p <.05. Kinetic analysis revealed a significantly (p <.01) reduced Vmax of T uptake on all experimental diets. The Km of uptake was not changed by vitamin D deficiency. These data indicate that the aminoaciduria of vitamin D deficiency is expressed at the brush border surface and that vitamin D deficiency is more important than plasma Ca level. This defect in T absorption is not altered by short-term vitamin D administration. BBMV uptake of glucose also was unchanged by vitamin D deficiency.
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Dabbagh, S., Chesney, R. & Gusowski, N. THE AMINOACIDURIA OF VITAMIN D DEFICIENCY IS EXPRESSED BY CHANGES AT THE BRUSH BORDER MEMBRANE. Pediatr Res 18, 360 (1984). https://doi.org/10.1203/00006450-198404001-01603