| [ Summary ] |
Many new insights into the molecular mechanisms of intestinal absorption of calcium, magnesium and phosphate have been made since the mid-1990s. These insights include the identification, cloning, and characterization of transmembrane proteins responsible for the absorption of all three of these nutrient molecules. The proteins identified with uptake of Ca2+ and Mg2+ across the apical membranes of enterocytes are members of the transient receptor potential (TRP) family of cation channels, on the other hand, intestinal phosphate absorption across the apical membrane is known to be mediated by a member of the sodium-phosphate cotransporter gene family (NaPi-IIb). Under conditions of high Ca2+/Mg2+ intake, Ca2+/Mg2+ may be absorbed throughout the entire length of the intestine, mainly through a paracellular pathway through tight junctions, which occurs between adjacent enterocytes. NaPi-IIb is considered to be a possible target for drug development for hyperphosphatemia. Clinically, several gastrointestinal diseases are known to affect bone metabolism. For example, gastrectomies, short bowel syndrome and inflammatory bowel disease lead to metabolic bone diseases. Several mechanisms such as malabsorption, changes in calciotropic, gastrointestinal or sex hormones, actions of inflammatory cytokines, and effects of therapeutic agents seem to underlie these bone diseases. Recently, it has been shown that serotonin produced by the intestines affects bone metabolism, further confirming the physiological connection between the intestinal tract and bone metabolism. |