title: Effects of stress simulated by dexamethasone on jejunal glucose transport in broilers.
abstract: Twenty-four 21-d-old Arbor Acres (AA) broilers with similar BW were randomly assigned into 4 groups to investigate the effects of stress on the absorption of glucose in the intestine of broilers and its mechanisms. In this study, dexamethasone (DEX), an analog to glucocorticoid secreted when animals suffer from stress, was chosen to simulate the effects of glucocorticoid. Broilers were injected subcutaneously with 0, 0.1, 1, or 5 mg of DEX/kg of BW into the abdomen for 7 d. To explain the nonspecific regulation of glucocorticoid on glucose transport of the jejunum in broilers, the effects of DEX on the jejunum mucosa morphology and disaccharidase activities in broilers were investigated. The results showed that DEX restrained the growth of broilers, and the extent of restraint increased with the increase of the dose of DEX (P<0.05). However, the activities of sucrase and maltase in the jejunum of the broilers injected with DEX were not different from those of the control broilers (P>0.05). In addition, DEX increased the crypt depth of jejunum in broilers, and decreased the villus height, absorption area, and villus height/crypt depth ratio significantly (P<0.05), whereas DEX had no significant effect on villus width and the thickness of mucosa lamina propria (P>0.05). To clarify the specific regulation of glucocorticoid on the glucose transport of jejunum in broilers, the absorption of glucose by jejunum brush border membrane vesicles (BBMV) was investigated, and the expression of Na+-dependent glucose transporter (SGLT1) mRNA was detected by real-time PCR. The results showed that DEX significantly inhibited the glucose absorption of jejunum BBMV (P<0.05), and the extent of inhibition depended on the dose of DEX. In addition, DEX decreased the expression of SGLT1 mRNA significantly (P<0.05). According to these data, we concluded that DEX restrains the glucose transport of jejunum in broilers through nonspecific and specific regulations.
authors.affiliation: Feed Research Institute, Chinese Academy of Agricultural Sciences, Beijing, China, 100081.
authors.forename: Y
authors.initials: Y
authors.lastname: Li
authors.forename: H Y
authors.initials: HY
authors.lastname: Cai
authors.forename: G H
authors.initials: GH
authors.lastname: Liu
authors.forename: X L
authors.initials: XL
authors.lastname: Dong
authors.forename: W H
authors.initials: WH
authors.lastname: Chang
authors.forename: S
authors.initials: S
authors.lastname: Zhang
authors.forename: A J
authors.initials: AJ
authors.lastname: Zheng
authors.forename: G L
authors.initials: GL
authors.lastname: Chen
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001835:Body Weight / Q000187:drug effects; D002645:Chickens / Q000254:growth & development / Q000502:physiology*; D003907:Dexamethasone / Q000494:pharmacology*; D005786:Gene Expression Regulation / Q000187:drug effects; D005947:Glucose / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000187:drug effects / Q000201:enzymology; D007583:Jejunum / Q000187:drug effects* / Q000378:metabolism*; D008871:Microvilli / Q000187:drug effects / Q000378:metabolism; D011897:Random Allocation; D051269:Sodium-Glucose Transporter 1 / Q000378:metabolism; D051297:Sodium-Glucose Transporter 2 / Q000378:metabolism; D013312:Stress, Physiological; D013997:Time Factors
chemical_list: D000893:Anti-Inflammatory Agents; D051269:Sodium-Glucose Transporter 1; D051297:Sodium-Glucose Transporter 2; D003907:Dexamethasone; D005947:Glucose