Dietary maltitol increases calcium content and breaking force of femoral bone in ovariectomized rats.

Maltitol is a disaccharide alcohol generated by hydrogenation of maltose and exhibiting resistance to intestinal disaccharidases. We demonstrated previously that maltitol stimulates transepithelial transport of calcium in the ileum, accompanied by an elevation of intestinal calcium absorption as well as calcium retention in the body. In this study, we examined whether the maltitol-induced increase in intestinal calcium absorption leads to an alteration of the physical properties of bones in rats subjected to ovariectomy. We used this study as a simulation model for postmenopausal females who are at risk for osteoporosis. Following the intake of a low-calcium diet for 28 d ovariectomized rats were fed diets containing either 10% maltose (control) or 10% maltitol, together with increased amounts of calcium (0.3% in Experiment 1 and 1.2% in Experiment 2) for 21 d. Balance studies performed during the final 5-d (Experiment 1) or 2-d (Experiment 2) period of the experiments showed that maltitol increased intestinal calcium absorption and retention. The breaking force of femoral bones was significantly elevated (by 5-7%) in animals fed the maltitol diet compared with that in rats fed the maltose diet. The calcium content in the femoral bones as well as the mineral bone density of the tibial metaphysis was also elevated in rats fed the maltitol diet. These results indicate that maltitol stimulates the intestinal absorption of dietary calcium leading to an increase in calcium content in the bone, and coinciding with the elevation of the breaking strength of the bone in ovariectomized rats.