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

Abstract

In a 36-d experiment, 32 pigs were depleted of Zn (24 d) using a soy-isolate (basal) diet (17 mg/kg of Zn) and then fed the basal diet (12 d) supplemented with 45 mg/kg of Zn from ZnSO4 (purified zinc sulfate dry powder, ZnSO4.nH2O) or from a Zn amino acid chelate (ZnAAC) to study the effectiveness of these dietary Zn sources in restoring serum and soft tissue Zn concentrations. Concurrently, nondepleted pigs were pair-fed both Zn-supplemented diets (eight pigs per diet) throughout the experiment. Serum Zn concentrations and serum alkaline phosphatase (ALP) activity of pigs fed the diets with no supplemental Zn were lower (P < .05) than those of nondepleted pigs after 7 and 14 d, respectively. After 24 d, concentrations of Zn in liver, pancreas, kidney, brain, and small intestine of Zn-depleted pigs were lower (P < .01) than those of nondepleted pigs. Except for decreased (P < .001) kidney Cu, soft tissue Cu and Fe concentrations were not affected by Zn status or Zn source. From d 24 to 36 (Zn repletion), serum and tissue Zn concentrations and serum ALP activities increased (P < .05), but the response was similar for both Zn sources in Zn-depleted and nondepleted pigs. At d 30 and 36, kidney Cu was increased (P < .01) in Zn-depleted pigs fed 45 mg/kg of Zn as either ZnSO4 or ZnAAC. Furthermore, Fe concentration was higher (P < .05) in intestinal segments of Zn-depleted and nondepleted pigs fed ZnAAC than in pigs fed ZnSO4. Accumulations of Cu in the kidney and Fe in the small intestine were affected by depletion and repletion of Zn and by dietary Zn source, respectively. In conclusion, serum and soft tissue Zn concentrations were clearly affected by Zn status: however, an effect of Zn source was not observed.