Abstract
Despite the widely known fact that low concentrations of extracellular free calcium can induce parathyroid hormone (PTH) secretion, the molecular mechanisms of such regulation and eventual calcium metabolism are not yet completely understood. The traditional view of calcium homeostasis is believed to be maintained by sensing changes in extracellular calcium in several distinct cell types, to stimulate the secretion of PTH, vitamin D and calcitonin, depending on the requirement of the body. These calciotropic hormones then act on the calcium-translocating cells of the kidney, bone and intestine to restore calcium balance [1]. New insights into calcium homeostasis were gained from a recent study by Imura et al.; the investigators proposed that low extracellular free calcium can induce PTH secretion through the klotho- and Na+,K+-adenosine triphosphatase (Na+,K+-ATPase)-dependent process [2].