The effect of dietary zinc depletion and repletion on rats: Zn concentration in various tissues and activity of pancreatic γ-glutamyl hydrolase (EC3.4.22.12) as indices of Zn status

Abstract

Unlike severe zinc deficiency, marginal Zn deficiency is difficult to identify in rats because no reliable indicator of suboptimal Zn status is currently available. We have previously observed reduced pancreatic γ-glutamyl hydrolase (EC3.4.22.12) activity and impaired pteroylpolyglutamate absorption in Zn-deficient rats. In the present study the effect of Zn depletion and repletion on the Zn concentration of various tissues and on the activity of this enzyme was investigated. The objective was to determine the sensitivity of these variables to Zn depletion and to evaluate their usefulness as indices of Zn status. Male Wistar rats (about 180 g), maintained from weanling on a purified Zn-adequate diet, were randomly allocated into twelve groups. A pretreatment control group was killed immediately. The remaining eleven groups were fed on a Zn-deficient diet and a group killed daily for 7 d (Zn-depleted groups). The remaining four groups were re-fed the Zn-adequate diet and a group killed daily (Zn-repleted groups). On analysis, pancreas and spleen Zn levels responded most rapidly to reduced Zn intake, followed by tibia, liver, kidney and plasma. Zn concentration was maintained in testes. Reduced plasma folate levels were also observed. A significant reduction in pancreatic γ-glutamyl hydrolase activity before the depletion of many tissue Zn stores confirms the Zn sensitivity of the enzyme. It was concluded that future investigation into the inter-relationship between Zn and folate metabolism may be useful in identifying a sensitive, biochemical index of Zn status.

Effectiveness of a zinc amino acid chelate and zinc sulfate in restoring serum and soft tissue zinc concentrations when fed to zinc-depleted pigs.

“…Although not measured in our study, bone also is severely depleted of Zn in Zn-deficient animals (Giugliano and Millward, 1984;Hill et al, 1986). Muscle, spleen, thymus, and testis, however, maintain their Zn concentrations during Zn deficiency (Crofton et al, 1983;Giugliano and Millward, 1984;Canton and Cremin, 1990). It may be that the most severely Zn-depleted tissues contain a relatively larger portion of the body Zn reserve.…”

“…Zinc-depleted pigs fed diets supplemented with 45 mg/ kg of Zn as either ZnSO 4 or ZnAAC were able to restore most of their serum and tissue Zn concentrations within 6 d. A fast replenishment of blood and tissue Zn concentrations was also observed in Zndeficient guinea-pigs and rats fed diets containing Zn levels that met or were in excess of the Zn requirement of the experimentally depleted animals (Roth and Kirchgessner, 1974;Gupta et al, 1989;Canton and Cremin, 1990;. Also, in our preliminary study (Swinkels and Kornegay, unpublished data), Zn-depleted pigs fed diets supplemented with 45 mg/kg of Zn as either ZnSO 4 or ZnAAC had a fast recovery of serum Zn levels and ALP activities that reached levels of nondepleted pigs by 6 to 9 d; liver and kidney Zn concentrations also increased during the 24-d repletion.…”

Zinc: Health Effects and Research Priorities for the 1990s

“…This loss of zinc is associated with more than a 50% decrease in the activity of y-glutamyl hydrolase in pancreatic tissue (265). Rapid loss in activity of pancreatic carboxypeptidase, a zinc metalloenzyme, has been demonstrated under similar conditions (266).…”

Zinc absorption and excretion in adult rats at zinc deficiency induced by dietary phytate additions: I. Quantitative zinc metabolism of 65Zn‐labelled adult rats at zinc deficiency

“…This may reflect the fact that these amounts of Zn had to be provided by mobilization from tissue Zn at fairly exhausted Zn storage (WINDISCH and KIRCHGESSNER 1999). Assuming that the endogenous Zn secretion is required for enzymatic digestion (CANTON and CREMIN 1990;VAN WOUWE and UIJLENBROEK 1994), the amounts of Zn actually secreted by the Zn-deficient animals were presumably too small to maintain normal digestion processes. This might have contributed to the depression of food intake.…”