Renal transport of taurine adapts to perturbed taurine homeostasis.

Renal adaptation apparently contributes to the homeostasis of taurine, a beta-amino compound that behaves as a conserved metabolite in the mammal. We studied two strains of inbred mice: C3H/HeJ (low-taurine excreter) and C57BL/6J (high-taurine excreter due to impaired basolateral membrane permeability to taurine). Low-protein and low-sulfur amino acid diets fed for two weeks significantly decreased plasma taurine in both strains, decreased fractional taurine excretion in vivo (particularly in the C57BL strain), and increased net uptake of taurine by renal cortex slices and isolated brush-border membrane vesicles (BBMV) in vitro in both strains. Renal adaptation was less obvious in vivo in the low-taurine excreter C3H strain, but in vitro adaptation, as observed in slices and BBMV (P less than 0.01), was greater than that observed in the C57BL strain. Renal cellular taurine content fell (P less than 0.01) only in the adapted C3H strain. The in vitro adaptive response was not confined to taurine; BBMV uptake of D-glucose and L-alanine was also enhanced in the adapted state. Specificity of the stimulus for adaptation was tested with a low-phenylalanine diet; a modest adaptation was observed in vivo and in vitro but only in the C3H strain. BBMV adaptation did not correlate with blood methionine but correlated inversely with plasma taurine (r = 0.71, P less than 0.05), implying that change in extracellular taurine may be a signal for renal adaptation in taurine homeostasis in the mammal.