In collaboration with Dr. Boyd O'Dell we have examined the cellular
role of zinc that mediates the inhibition of food intake and growth
seen with zinc deficiency. In cell lines, we found evidence that
zinc depletion prevents IGF-1 signaling associated with cell division.
We have observed that maintaining circulating IGF-1 concentrations
in rats with mini-osmotic pumps during zinc depletion failed to
prevent growth inhibition, or anorexia. Rats fed zinc-deficient
diets become anorexic within 4 days. We found that administration
of megestrol acetate improved food intake, but not growth in zinc-depleted
rats. Furthermore, rats fed zinc deficient diets failed to respond
(increase food intake) to intracerebral ventricular injection of
neuropeptide Y, suggesting a potential defect in this signaling
pathway.
In current work we are collaborating with Dr.
Bernhard Hennig, University of Kentucky on a project related
to the role of zinc in the immune system.