Acrodermatitis Enteropathica*

Entwisle, B. R.

doi:10.1111/j.1440-0960.1965.tb01365.x

Cited by 13 publications

(2 citation statements)

References 28 publications

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“…In children affected with acrodermatitis enteropathica, an inherited disease that affects zinc metabolism (8), the symptoms characteristic of the disease do not generally appear until the child is weaned from the breast (1, 4,5). Human milk has also been used successfully in the treatment of acrodermatitis enteropathica (15).…”

Section: Speculationmentioning

confidence: 99%

Characterization and Quantitation of a Zinc-Binding Ligand in Human Milk

Evans

Johnson

1980

Pediatric Research

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SummaryA low-molecular-weight zinc-binding ligand from human milk has been isolated and characterized. The ligand was isolated by chromatography on Dowex 50, Dowex 1, and Sephadex G-15 equilibrated with 0.153 mM Zn(N03)2. Mass spectroscopy, thinlayer chromatography, and infrared spectroscopy proved that the zinc-binding ligand isolated by this method from human milk is pyridine-2-carboxylic acid, commonly known as picolinic acid. The concentration of picolinic acid in human milk was 308 pM, the concentration in one brand of processed cow's milk was 20 pM, but picolinic acid was undetectable in a second brand of cow's milk and in four different infant formulas. Weanling rats fed supplemental picolinic acid absorbed significantly more dietary zinc and gained significantly more weight than rats fed an unsupplemented diet. The results suggest that the high bioavailability of zinc in human milk results from the presence of picolinic acid, a bidentate chelating ligand which facilitates zinc absorption from the intestine. SpeculationThe high bioavailability of zinc in human milk results from the presence of picolinic acid, a bidentate chelating ligand which facilitates zinc absorption from the intestine.Several clinical observations demonstrate that the bioavailability of zinc from human milk is much greater than that from cow's milk. In children affected with acrodermatitis enteropathica, an inherited disease that affects zinc metabolism (8), the symptoms characteristic of the disease do not generally appear until the child is weaned from the breast (1, 4, 5). Human milk has also been used successfully in the treatment of acrodermatitis enteropathica (15). Hambidge et al. (9) found that the plasma zinc concentration of breast-fed infants is not significantly different than that of healthy young adults. In contrast, the plasma zinc concentration of infants fed either zinc-supplemented formula or non-zinc-supplemented formula is significantly less than that of young adults. These observations suggest that human milk may contain a ligand or ligands which facilitate zinc absorption.To date, attempts to isolate zinc-binding ligands from biologic fluids have not been successful due to the fact that investigators have consistently used classical gel filtration chromatography. The problems encountered when attempting to detect and identify zinc-chelating ligands by the use of classical gel filtration have been discussed by Evans et al. (6). These authors have also described a technique, referred to as modified gel filtration chromatography, which can be used to reproducibly detect zinc-binding ligands in biologic fluids. This technique has now been adapted to isolate and quantitate a zinc-binding ligand in human milk. MATERIALS AND METHODS DETECTION OF ZINC-BINDING LIGANDSified gel filtration chromatography. A glass column 1.5 x 90 crr was packed with 44.4 g Sephadex G-15 (Pharmacia Fine Chemi. cals, Inc.) (18). The gel was equilibrated with 50 mM Tris acetate pH 7.4, that contained 0.1% NaN3 and 0.153 mM Zn(NO3)z. Thc buffer...

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Section: Speculationmentioning

confidence: 99%

Characterization and Quantitation of a Zinc-Binding Ligand in Human Milk

Evans

Johnson

1980

Pediatric Research

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“…The pathogenesis of the disease is not koown. The following theories have been proposed: transition from breast to artificial feeding, since the first clinical symptoms usually appear at this time (3,7,20); disorders in the intestinal absorption of tryptophan (6); formation of toxic peptides from undigested proteins as a result of deficiency of leucine-aminopep tidase (14); disorders of. tryptophan metabolism in the kynurenine and xanthureaic acid pathway (I, 11, 1 S); and disorders of lipid absorption and meta bolism (2,4,16,18,27).…”

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confidence: 99%