[Role of advanced glycation endproducts in adynamic bone disease].

To clarify the role of AGEs in adynamic bone disease, we investigated the effect of these substances on cultured human osteoblasts and parathyroid cells. AGEs-BSA significantly inhibited parathyroid hormone secretion in response to the low calcium concentration. In HEK-293 cells, expressing calcium-sensing receptors, the same AGE concentration caused a significant potentiation of the extracellular Ca(2+) induced-intracellular calcium concentration. AGEs significantly inhibited the synthesis of type I collagen and osteocalcin in response to stimulation with 1,25(OH)(2)D(3). These data suggest that AGEs are involved in the pathogenesis of adynamic bone disease by inhibiting PTH secretion in response to hypocalcemia and by inhibiting osteoblastic activity.