Most minerals are absorbed by carrier-mediated diffusion into intestinal mucosal cells and accumulated by binding to intracellular proteins. There is then sodium-dependent active transport from the epithelial cells into the bloodstream, where again they are usually bound to transport proteins. Genetic defects of the intracellular binding proteins or the active transport systems at the basal membrane of the mucosal cell can result in functional deficiency despite an apparently adequate intake of the mineral.
The absorption of many minerals is affected by other compounds present in the intestinal lumen. As discussed in section 4.5.1, a number of reducing compounds can enhance the absorption of iron, and a number of chelating compounds enhance the absorption of other minerals. For example, zinc absorption is dependent on the secretion by the pancreas of a zinc-binding ligand (tentatively identified as the tryptophan metabolite picolinic acid). Failure to synthesize and secrete this zinc-binding ligand as a result of a genetic disease leads to the condition of acrodermatitis enteropathica — functional zinc deficiency despite an apparently adequate intake.
Diets based on unleavened wheat bread contain a relatively large amount of phytic acid (inositol hexaphosphate), which can bind calcium, iron and zinc to form insoluble complexes that are not absorbed. Phytases in yeast catalyse dephosphorylation of phytate to products that do not chelate the minerals.
Polyphenols (section 188.8.131.52), and especially tannic acid in tea, can also chelate iron and other minerals, reducing their absorption, and large amounts of free fatty acids in the gut lumen (associated with defects of fat absorption; section 4.3.2) can impair the absorption of calcium and magnesium, forming insoluble soaps.
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