The requirement of zinc for the growth of numerous organisms, ranging from bacteria to humans, is well established. Growth failure is a relatively early consequence of zinc deficiency in experimental animals. Given the lack of a zinc store, in the absence of a sufficient dietary supply zinc will be immediately unavailable for new tissue. Numerous processes seem to contribute to the growth failure. Experiments in animals have shown that zinc deficiency leads to a drop in food intake, though the use of control animals pair-fed an identical amount of a zinc-sufficient diet demonstrates a clear role for a lack of zinc beyond its effects on feeding behavior. The endocrine system is involved with multiple effects of zinc deficiency on the somatotrophic axis, notably a reduction in circulating concentrations of insulin-like growth factor 1 (IGF-1). Again, this appears to be only part of the story since forcefeeding a zinc-deficient diet and administering exogenous IGF-1 both fail to correct the growth failure caused by zinc deficiency. Growth of cultured cells is dependent on media zinc. DNA synthesis is interrupted. Production of thymidine kinase mRNA is diminished by the removal of zinc, but again this appears to be only a partial explanation. The IGF-1 signalling pathway within cells also seems to be affected. Zinc is also required for wound healing, presumably owing to related processes.

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