Abstract
This study was conducted to investigate the effect of dietary zinc from different sources on growth performance, intestinal health and zinc metabolism of broilers challenged with necrotic enteritis (NE). 432 one day-old Arbor Acres (AA) male broilers were divided into three dietary treatments: NT group (basal diet), OT group (basal diet with 60mg/kg zinc glycinate), IT group (basal diet with 60mg/kg zinc sulfate), with 12 replicates of 12 broilers per treatment. Half of the replicates of each dietary treatment were subjected to NE challenge from day 23. The animal experiment lasted 35 days. The results showed that NE challenge increased feed conversion ratio (FCR) in broilers from 22-35 days and zinc glycinate decreased FCR from 1-21 days. Zinc glycinate significantly reduced intestinal lesion scorings in the duodenum and ileum under NE challenge, and both sources of zinc attenuated intestinal permeability under challenge condition. In addition, NE challenge mediated zinc transporter proteins and metallothionein (MT) to regulate systemic zinc homeostasis, as reflected by the fact that NE challenge up-regulated the gene expressions of jejunal ZnT1, Zip8, Zip14, and MT, and the level of the liver ZnT1. Zinc glycinate increased ZnT1 gene expression in the liver under challenge, and both sources of zinc reduced gene expression levels of Zip8 in the liver. These modifications were responsible for the down-regulation of zinc levels in serum, tibia, pectoral muscle and cecum content under NE challenge and the up-regulation of zinc level in the liver, whereas zinc glycinate showed positive effects on zinc levels in serum, tibia, pectoral muscle and liver. In conclusion, NE challenge led to inflammatory damage and oxidative stress in broilers, disrupting gut barrier function, reducing growth performance and leading to the remodeling of zinc homeostasis. Dietary zinc alleviated NE challenge-induced oxidative stress and intestinal inflammation, and zinc glycinate showed better results in decreasing the FCR and improving the intestinal barrier function.