The role of certain amino acids, dipeptides and organic acids as ligands to facilitate the intestinal absorption of zinc was investigated by using an in vivo procedure on ileal segments of adult rats. Ligand:zinc ratios equal to or less than 3:1 were optimal for amino acids and dipeptides such as L-glutamate, glycine, L-histidine, L-tryptophan and glycylglycine. An excess of ligand reduced zinc absorption. At a 130:1 L-histidine:zinc ratio the absorption of zinc was less than one-fourth that obtained at a 3:1 ratio. Picolinate was a less effective ligand. The kinetics of the complex L-histidine:zinc at a 2:1 ratio and at pH 7.5 were determined in the absence and presence of a 20 mM excess of amino acid in a zinc concentration range between 0.038 mM and 6.00 mM. In both cases the Vmax was 2200 pmol/(minute . cm), but the Kt increased from 0.54 mM to 1.46 mM in the presence of the L-histidine excess. These data suggest a competitive inhibition of the L-histidine:zinc complex by the amino acid. Such an effect was dependent on the stereoisomerism of histidine, since the unnatural D-isomer was far less effective than the natural L-isomer in facilitating zinc absorption. The presence of an intact protein (bovine serum albumin) sharply decreased the ileal absorption of the L-histidine:zinc complex.

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Zinc status was studied in 30 patients with chronic inflammatory bowel disease (CIBD) as well as in 17 normal children, 13 primordial short stature, and 17 anorexia nervosa patients. Basal serum and urinary excretion levels of zinc were measured in all patients. In addition, a zinc loading test was performed in 16 CIBD patients, 21 normal and/or short stature children, and nine patients with anorexia nervosa. Eleven of 30 patients with CIBD had serum zinc values less than 0.7 microgram/ml, whereas none of the other patients had hypozincemia. In addition, the mean urinary zinc excretion of CIBD patients was significantly lower than that of patients with primordial short stature and with anorexia nervosa. An altered response to oral zinc load was the most frequent abnormality in CIBD patients. Those with moderate and severe clinical disease activity had a decreased serum rise of zinc after the oral load of this ion. Urinary excretion of zinc after oral load was also marked by deficiency in all CIBD patients. The abnormalities of zinc metabolism were more frequent among the CIBD patients with growth abnormalities, although they were also found in patients who had normal growth. Among the 14 patients with CIBD and growth abnormalities, seven were hypozincemic and four hypozincuric. Hypozincemia was only found in four patients who had normal height; however, the growth velocity was not known. The zinc tolerance test revealed abnormalities in four of five CIBD patients with short stature and in two of three patients with slow growth. On the other hand, similar alterations in zinc tolerance tests were seen in three of seven CIBD patients with normal height and growth.