| Abstract: | This study investigated the different addition levels of iron (Fe) in growing-finishing pigs and the effect of different Fe levels on growth performance, hematological status, intestinal barrier function, and intestinal digestion. A total of 1,200 barrows and gilts (Large White × Landrace] × Duroc) with average initial body weight (BW; 27.74 ± 0.28 kg) were housed in 40 pens of 30 pigs per pen (gilts and barrows in half), blocked by BW and gender, and fed five experimental diets (eight replicate pens per diet). The five experimental diets were control diet (basal diet with no FeSO4 supplementation), and the basal diet being supplemented with 150, 300, 450, or 600 mg/kg Fe as FeSO4 diets. The trial lasted for 100 d and was divided into the growing phase (27 to 60 kg of BW) for the first 50 d and the finishing phase (61 to 100 kg of BW) for the last 50 d. The basal diet was formulated with an Fe-free trace mineral premix and contained 203.36 mg/kg total dietary Fe in the growing phase and 216.71 mg/kg in the finishing phase based on ingredient contributions. And at the end of the experiment, eight pigs (four barrows and four gilts) were randomly selected from each treatment (selected one pig per pen) for digesta, blood, and intestinal samples collection. The results showed that the average daily feed intake (P = 0.025), average daily gain (P = 0.020), and BW (P = 0.019) increased linearly in the finishing phase of pigs fed with the diets containing Fe. On the other hand, supplementation with different Fe levels in the diet significantly increased serum iron and transferrin saturation concentrations (P < 0.05), goblet cell numbers of duodenal villous (P < 0.001), and MUC4 mRNA expression (P < 0.05). The apparent ileal digestibility (AID) of amino acids (AA) for pigs in the 450 and 600 mg/kg Fe groups was greater (P < 0.05) than for pigs in the control group. In conclusion, dietary supplementation with 450 to 600 mg/kg Fe improved the growth performance of pigs by changing hematological status and by enhancing intestinal goblet cell differentiation and AID of AA. |
