Dietary supplementation with zinc oxide increases Igf-I and Igf-I receptor gene expression in the small intestine of weanling piglets

This study was conducted to investigate the mechanism for the effect of elevated levels of dietary zinc oxide (ZnO) in enhancing the intestinal growth of weanling piglets. In Experiment 1, 4-wk-old (8.1 +/- 0.6 kg) crossbred barrows (n = 36) were assigned randomly to 1 of the 2 dietary groups, with 6 pens/group (3 pigs/pen). One group was fed the basal diet containing 100 mg Zn/kg diet. The other group was fed the basal diet supplemented with ZnO to provide 3000 mg Zn/kg diet. Pigs consumed their feed ad libitum for 14 d. In Experiment 2, 4-wk-old (7.6 +/- 0.16 kg) crossbred barrows (n = 16) were housed individually and assigned to 1 of the 2 dietary groups (8 pigs/group) as in Experiment 1, except that the 2 groups were pair-fed the same amount of feed. At the end of a 14-d treatment period, all of the pigs in both Experiments 1 and 2 were weighed, feed consumption was measured, and blood samples were collected for assays of insulin-like growth factor-I (IGF-I). In addition, 1 pig from each pen in Experiments 1 and 2 was selected randomly to obtain the small-intestinal mucosa for analyzing IGF-I and IGF-I receptor (IGF-IR) gene expression and to determine the small-intestinal morphology. In Experiment 1, dietary supplementation of ZnO increased (P < 0.05) the daily body weight gain and daily feed intake. In Experiment 2, dietary supplementation of ZnO increased (P < 0.05) the daily body weight gain and feed conversion efficiency. In both experiments, the villous height of the small-intestinal mucosa and both the mRNA and protein levels for IGF-I and IGF-IR in the small intestine were markedly enhanced (P < 0.05) by feeding elevated levels of Zn. Serum IGF-I levels did not differ between the control and Zn-supplemental groups in either experiment. Collectively, these results suggest that dietary Zn supplementation exerts its beneficial effects on the intestinal growth of weanling piglets through increasing IGF-I and IGF-IR expression in the small-intestinal mucosa.