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The reduced capability of the tubular Pi transport to adapt to a high Pi diet in TPTX rats can be normalized by physiological doses of 1,25-(OH)2D3. This suggests that the chronic consequence of a lack of PTH could be due, at least in part, to the reduced production of 1,25-(OH)2D3. The mechanism of Pi adaptation appears to be the most important regulator of Pi excretion in the growing rats, since it can markedly alter the acute phosphaturic response to parathyroid hormone.
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