Molecular Regulation of Calcium Metabolism

In the other chapters in this book, it is apparent that bone is the tissue that is affected during periods of inadequate dietary calcium intake, as a result of changes in physiology or defects in calcium homeostasis. Based on this, one might reasonablybut incorrectly—believe that calcium homeostasis is regulated to maintain bone integrity. As Fig. 1 illustrates, and as Chapter 10 developed in some detail, bone, intestine, and kidney make up a three-tissue axis whose activities are coordinated to maintain serum calcium within a narrow range (8.9–10.2 mg/dL). In this model, calcium absorption from the intestine is a disturbing signal that elevates serum calcium after a meal while turnover (i.e., the balance between bone formation and resorption) and renal calcium excretion are controlling signals that respond to fluxes in serum calcium. The import of this coordinated regulation can be seen in the table accompanying Fig. 1. This table is based on research by Bronner and Aubert who studied the influence of dietary calcium on calcium homeostasis in growing rats (). Using calcium kinetics, their studies showed that when calcium intake is inadequate (a lack of Ca input into serum Ca), the body compensates by increasing calcium mobilization from the bone (resorption) as well as the efficiency of both calcium reabsorption from the renal filtrate and calcium absorption from the diet. Similar types of compensatory adaptation would also occur if renal calcium output was too high (e.g., as a result of high dietary salt intake), leading to a drain on serum Ca that promotes compensation at the intestine and bone, or if bone resorption were elevated (e.g., owing to the loss of estrogen), leading to elevated serum Ca that would suppress the activities of the intestine and bone.