Intestinal Ca(2+) absorption revisited: A molecular and clinical approach

Ca(2+) has an important role in the maintenance of the skeleton and is involved in the main physiological processes. Its homeostasis is controlled by the intestine, kidney, bone and parathyroid glands. The intestinal Ca(2+) absorption occurs mainly via the paracellular and the transcellular pathways. The proteins involved in both ways are regulated by calcitriol and other hormones as well as dietary factors. Fibroblast growth factor 23 (FGF-23) is a strong antagonist of vitamin D action. Part of the intestinal Ca(2+) movement seems to be vitamin D independent. Intestinal Ca(2+) absorption changes according to different physiological conditions. It is promoted under high Ca(2+) demands such as growth, pregnancy, lactation, dietary Ca(2+) deficiency and high physical activity. In contrast, the intestinal Ca(2+) transport decreases with aging. Oxidative stress inhibits the intestinal Ca(2+) absorption whereas the antioxidants counteract the effects of prooxidants leading to the normalization of this physiological process. Several pathologies such as celiac disease, inflammatory bowel diseases, Turner syndrome and others occur with inhibition of intestinal Ca(2+) absorption, some hypercalciurias show Ca(2+) hyperabsorption, most of these alterations are related to the vitamin D endocrine system. Further research work should be accomplished in order not only to know more molecular details but also to detect possible therapeutic targets to ameliorate or avoid the consequences of altered intestinal Ca(2+) absorption.