Changes in the extracellular concentration of inorganic phosphate (Pi) modulate cellular function in a physiologically relevant manner. High serum Pi leads to an increase in PTH secretion, PTH mRNA stability, and parathyroid cell (PT) proliferation. The reduced Pi reabsorption is achieved by a removal of type II a NaPi co-transporter from apical membrane. Acute internalization in response to high dietary Pi-intake or administration of PTH is via clathrin-coated structures and is followed by subsequent lysosomal degradation. In this review, the effects of PTH on the metabolism of Pi are discussed.