Zinc metabolism - an outline

As with other essentiai nutrients there are homeostatic mechanisms which maintain a constant tissue concentration of zinc in spite of fiuctuations in dietary suppiy. The total dietary intake is 10-15 mg per day. The bioavailability of zinc from different foodstuffs varies. Some 40% of zinc is absorbed from the average diet. Inside the intestinai mucosai ceil zinc enters a metabolic pooi in equiiibrium with zinc-thionein. The synthesis of this metal binding protein is induced by various metals, and it appears to reguiate their intracellular transport. Zinc leaves the intestinal mucosal cell across the plasma membrane and is taken up by albumin in the portal circulation. The liver extracts zinc with a high 

Zinc is excreted from the body primarily in the faeces. There is a substantial en-terohepatic re-circulation, and as Cousins (1982) notes, the gut gets two zinc meals per day, one from foodstuff, the other from zinc re-entering the intestinal lumen in digestive juices and crossing the mucosal barrier from the plasma zinc-albumin complex. The total zinc output in faeces usually equals the dietary intake at around 10-15 mg per day. 

Urinary excretion of zinc is much smaller at 0.5 mg zinc per day. Urinary output does not increase as dietary zinc intake rises. 

It is important to distinguish between changes in zinc metabolism which occur as a secondary effect of disease, injury, infection and drug therapy and alterations caused by a primary nutritional zinc deficiency. There is confusion in the literature because a number of unrelated causes can temporarily lower the concentration of zinc in plasma, and this is reported uncritically as evidence of nutritional depletion. Since a high proportion of zinc in plasma is albumin bound, any circumstance which lowers plasma albumin wiil also lower plasma zinc. For example, the changes seen in severe liver disease are primarily caused by a failure of hepatic synthesis of plasma proteins such as albumin. This results in problems in the distribution of zinc and eventual tissue depletion. It is questionable whether zinc supplementation of diet is worthwhile without some restoration of hepatocyte function, by effective treatment of the underlying disease (Mills et al., 1983). 

Serious disease of the intestinal tract may disturb zinc absorption and increase faecal zinc excretion. Inflammatory bowel disease with persistent diarrhoea as in Crohn s Disease could have complicating features due to a secondary zinc deficiency (Sandstead, 1982). 

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