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Abstract
The inhibition of growth is a cardinal symptom of zinc deficiency. In animals fed
a zinc-inadequate diet, both food intake and growth are reduced within 4-5 d. Despite
the concomitant reduction in food intake and growth, reduced energy intake is not
the limiting factor in growth, because force-feeding a zinc-inadequate diet to animals
fails to maintain growth. Hence, food intake and growth appear to be regulated by
zinc through independent, although well coordinated, mechanisms. Despite the long-term
study of zinc metabolism, the first limiting role of zinc in cell proliferation remains
undefined. Zinc participates in the regulation of cell proliferation in several ways;
it is essential to enzyme systems that influence cell division and proliferation.
Removing zinc from the extracellular milieu results in decreased activity of deoxythymidine
kinase and reduced levels of adenosine(5')tetraphosphate(5')-adenosine. Hence, zinc
may directly regulate DNA synthesis through these systems. Zinc also influences hormonal
regulation of cell division. Specifically, the pituitary growth hormone (GH)-insulin-like
growth factor-I (IGF-I) axis is responsive to zinc status. Both increased and decreased
circulating concentrations of GH have been observed in zinc deficiency, although circulating
IGF-I concentrations are consistently decreased. However, growth failure is not reversed
by maintaining either GH or IGF-I levels through exogenous administration, which suggests
the defect occurs in hormone signaling. Zinc appears to be essential for IGF-I induction
of cell proliferation; the site of regulation is postreceptor binding. Overall, the
evidence suggests that reduced zinc availability affects membrane signaling systems
and intracellular second messengers that coordinate cell proliferation in response
to IGF-I.