Trace element metabolism is regulated by numerous factors which are dependent on availability of nutrients and on the integrity of the gastrointestinal tract and on liver function. It is well known that a diet rich in phytates can reduce zinc bioavailability while a diet rich in animal proteins results in much higher absorption (1). Zinc absorption is regulated homeostatically so that in zinc depleted diets a strong reduction in urinary and fecal zinc excretion is observed. Gastric acidity is essential for zinc absorption as it is for iron. In experiments conducted in healthy volunteers we showed a reduction in zinc absorption when cimetidine (400 mg) or ranitidine (300 mg) were administered (2) (Fig 1). Recently, the same results were obtained after famotidine (40 mg) administration (3). A reduction in zinc absorption has also been observed in the healthy elderly and this may support the evidence of marginal zinc deficiency reported in several studies (4). Zinc uptake appears to be mediated by low molecular weight intracellular ligands able to bind the metal at the brush border and transfer it into the cell. The suggested ligands are picolinic and citric acid and prostaglandins. Deficiency of citric acid has been described in chronic pancreatitis and we observed that zinc absorption reverted to normal after the administration of citric acid in a group of patients with chronic pancreatitis (5). Once in the cell, zinc is stored in metallothioneins and other cysteine-rich molecules which synthesis is stimulated by an excess of zinc in the diet.
KeywordsChronic Pancreatitis Zinc Deficiency Zinc Level Zinc Supplementation Short Bowel Syndrome
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