Affiliation:
1. Poultry Mineral Nutrition Laboratory, College of Animal Science and Technology, Yangzhou University, Yangzhou 225009, China
2. College of Animal Science and Technology, Hebei Normal University of Science and Technology, Qinhuangdao 066004, China
3. Mineral Nutrition Research Division, State Key Laboratory of Animal Nutrition, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing 100193, China
Abstract
A prior investigation revealed that a lack of Zinc (Zn) could hinder intestinal cell proliferation in broiler chickens; however, the mechanisms responsible for this effect remain unclear. We aimed to investigate the possible mechanisms of dietary Zn deficiency in inhibiting the jejunal cell proliferation of broilers. For this study, a total of 112 chickens (21 days old) were randomly divided into two treatments (seven replicate cages per treatment, eight chickens per replicate cage): the control group (CON) and the Zn deficiency group. The duration of feeding was 21 d. Chickens in the control group were provided with a basal diet containing an extra addition of 40 mg Zn/kg in the form of Zn sulfate, whereas chickens in the Zn deficiency group were given the basal diet with no Zn supplementation. The results indicated that, in comparison to the CON, Zn deficiency increased (p < 0.05) the duodenal and jejunal crypt depth (CD) of broilers on d 28 and jejunal and ileal CD on d 35, and decreased (p < 0.05) the duodenal, jejunal, and ileal villus height/crypt depth (VH/CD) on d 28 and the jejunal VH, jejunal and ileal villus surface area, and VH/CD on d 35. Furthermore, Zn deficiency decreased (p < 0.0001) the number of proliferating cell nuclear antigen-positive cells and downregulated (p < 0.01) the mRNA or protein expression levels of phosphatidylinositol 3-kinase (PI3K), phosphorylated PI3K, phosphorylated serine–threonine kinase (AKT), phosphorylated mechanistic target of rapamycin (mTOR), G protein-coupled receptor 39 (GPR39), and extracellular-regulated protein kinase, but upregulated (p < 0.05) the mRNA or protein expression levels of P38 mitogen-activated protein kinase, c-jun N-terminal kinase (JNK) 1 and JNK2, and phosphorylated protein kinase C in the jejunum of the broilers on d 42. It was concluded that dietary Zn deficiency inhibited cell proliferation possibly via the GPR39-mediated suppression of the PI3K/AKT/mTOR signaling pathway in the jejunum of broilers.
Funder
Jiangsu Shuang Chuang Tuan Dui program
Jiangsu Shuang Chuang Ren Cai program
Key International Cooperation Program of the National Natural Science Foundation of China
Reference45 articles.
1. Influence of dietary zinc, copper, and manganese on the intestinal health of broilers under eimeria challenge;Bortoluzzi;Front. Vet. Sci.,2020
2. Broiler live performance response to dietary zinc source and the influence of zinc supplementation in broiler breeder diets;Hudson;Anim. Feed. Sci. Technol.,2005
3. Chronic zinc deficiency alters chick gut microbiota composition and function;Reed;Nutrients,2015
4. Effects of higher levels of zinc supplementation on performance, mineral availability, and immune competence in broiler chickens;Sunder;J. Appl. Poult. Res.,2008
5. Effect of zinc level and source (zinc oxide vs. Zinc glycine) on bone mechanical and geometric parameters, and histomorphology in male ross 308 broiler chicken;Tomaszewska;Rev. Bras. Ciência Avícola,2017
Cited by
1 articles.
订阅此论文施引文献
订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献