Hyperzincuria in diabetics has been regarded as the culprit depleting body zinc stores. Studies were designed to assess rates of $\sp{65}$Zn absorption and retention as a possible compensation mechanism; to assess zinc concentrations and distribution among body compartments; and to assess the kinetics of $\sp{65}$Zn metabolism in STZ-diabetic rats. The rates of $\sp{65}$Zn absorption and retention were not significantly different between STZ-diabetic and control rats. However, STZ-diabetic rats had significantly higher rates of $\sp{65}$Zn absorption (16.88%) and retention (34.36%) when they were "Post-fasted" than when they were "Prior-fasted" (9.04% and 18.68% respectively). These differences were also present in control rats at a lesser degree (14.86% and 30.19% for "post-fasting" and 11.76% and 23.25% for "prior-fasting" respectively). This observation suggests that dietary pattern affects $\sp{65}$Zn absorption and retention. The results indicate also that STZ-diabetic rats are capable of absorbing and retaining enough zinc to meet body needs. The STZ-diabetic rats had higher zinc levels in all tissues analyzed when they were on diet adequate for zinc, with significant increases in liver, duodenum, pancreas and femur; they had significantly higher zinc levels in liver and muscle but decreased plasma zinc levels when fed the diet marginal for zinc; on zinc-supplemented diet, they had significantly higher zinc levels in liver, kidney, duodenum, muscle and femurs, but decreased plasma zinc levels. Plasma zinc levels, a common measure of zinc status, did not reflect dietary zinc intake of STZ-diabetics. Endogenous zinc secretion was not decreased as judged by measuring $\sp{65}$Zn in feces and duodenum. Whole body mean zinc concentrations (WBMZC) were significantly higher in STZ-diabetic rats on all three dietary zinc levels. This increased WBMZC in diabetes may be the result of both increased absorption and tissue catabolism during diabetes. One may conclude that to accommodate zinc from increased tissue catabolism, the liver functions to store and sequester zinc from the circulation; while the kidney is overloaded and secreted it. Hyperzincuria in diabetes in this regard is a salvage of increased body zinc level. The diabetic bone may have disorders in utilizing Zn during Zn deficiency as judged by its kinetics and decreased $\sp{65}$Zn specificity. The whole body mean concentrations of copper and iron of STZ-diabetics were also increased, suggesting similar disorders.

Thesis (M.S.P.H.)--University of Michigan, 1937.

Thesis (M.S.P.H.)--University of Michigan, 1940.

Thesis (M.P.H.)--University of Michigan, 1946.

Thesis (M.P.H.)--University of Michigan, 1945.

Thesis (M.P.H.)--University of Michigan, 1945.

Thesis (M.S.P.H.)--University of Michigan, 1940.

Thesis (M.P.H.)--University of Michigan, 1946.

Thesis (M.S.P.H.)--University of Michigan, 1937.

Thesis (M.P.H.)--University of Michigan, 1945.