Vitamins and minerals are released from food during digestion, although this is not complete, and the availability of vita mins and minerals depends on the type of food and, especially for minerals, the presence of chelating compounds. The fat soluble vitamins are absorbed in the lipid micelles that are the result of fat digestion; water-soluble vitamins and most mineral salts are absorbed from the small intestine either by active transport or by carrier-mediated diffusion followed by binding to intracellular proteins to achieve concentrative uptake. Vitamin B12 absorption requires a specific transport protein, intrinsic factor; calcium absorption is dependent on vitamin D; zinc absorption requires a zinc-binding ligand secreted by the exocrine pancreas, and the absorption of iron is limited (see following text).

Calcium Absorption Is Dependent on Vitamin D

 In addition to its role in regulating calcium homeostasis, vitamin D is required for the intestinal absorption of calcium. Synthesis of the intracellular calcium-binding protein, calbindin, required for calcium absorption, is induced by vitamin D. Vitamin D also acts to recruit calcium transporters to the cell surface, so increasing calcium absorption rapidly—a process that is independent of new protein synthesis.

Phytic acid (inositol hexaphosphate) in cereals binds calcium in the intestinal lumen, preventing its absorption. Other minerals, including zinc, are also chelated by phytate. This is mainly a problem among people who consume large amounts of unleavened whole-wheat products; yeast contains an enzyme, phytase, that dephosphorylates phytate, so rendering it inactive. High concentrations of fatty acids in the intestinal lumen, as a result of impaired fat absorption, can also reduce calcium absorption by forming insoluble calcium salts; a high intake of oxalate can sometimes cause deficiency since calcium oxalate is insoluble.

Iron Absorption Is Limited and Strictly Controlled, but Enhanced by Vitamin C and Alcohol

 Although iron deficiency is a common problem in both developed and developing countries, about 10% of the population are genetically at risk of iron overload (hemochromatosis), and in order to reduce the risk of adverse effects of nonenzymic generation of free radicals by iron salts, absorption is strictly regulated. Inorganic iron is transported into the mucosal cell by a proton-linked divalent metal ion transporter, and accumulated intracellularly by binding to ferritin. Iron leaves the mucosal cell via a transport protein ferroportin, but only if there is free transferrin in plasma to bind to. Once transferrin is saturated with iron, any that has accumulated in the mucosal cells is lost when the cells are shed. Expression of the ferroportin gene (and possibly also that for the divalent metal ion transporter) is downregulated by hepcidin, a peptide secreted by the liver when body iron reserves are adequate. In response to hypoxia, anemia, or hemorrhage, the synthesis of hepcidin is reduced, leading to increased synthesis of ferroportin and increased iron absorption (Figure1). As a result of this mucosal barrier, only ~10% of dietary iron is absorbed, and only 1 to 5% from many plant foods.

Fig1. Absorption of iron. Hepcidin secreted by the liver downregulates synthesis of ferroportin and limits iron absorption.

Inorganic iron is absorbed in the Fe2+ (reduced) state, and hence, the presence of reducing agents enhances absorption. The most effective compound is vitamin C, and while intakes of 40 to 80 mg of vitamin C per day are more than adequate to meet requirements, an intake of 25 to 50 mg per meal enhances iron absorption, especially when iron salts are used to treat iron deficiency anemia. Alcohol and fructose also enhance iron absorption. Heme iron from meat is absorbed separately and is considerably more available than inorganic iron. However, the absorption of both inorganic and heme iron is impaired by calcium—a glass of milk with a meal significantly reduces iron availability.

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