Abstract：
:Bile acids (BAs) are synthesized in the liver via the oxidation of cholesterol and further metabolized by microbiota in the gut, where they simultaneously impact gut function. In the present study, 10 goats were randomly divided into 2 groups; 1 group was injected with dexamethasone (Dex; 0.2 mg/kg), and the other group was injected with saline as the control (Con) for 21 d. Expression levels of key genes and proteins in the liver and gut mucosa were analyzed and compared to investigate the impact of chronic stress on BA metabolism and related functions in ruminants. The results revealed that Dex decreased plasma total BAs (TBAs) concentration (P < 0.05) but increased TBA concentration in the cecal digesta (P < 0.05). Total cholesterol in the liver decreased moderately in response to Dex. The protein expression of cytochrome P450 family 7 subfamily A member 1 and cytochrome P450 family 27 subfamily A member 1, 2 enzymes that control BA synthesis in the liver, remained unchanged by Dex administration (P > 0.05). The expression of several genes in the cecal mucosa encoding epithelial tight junction proteins, including occludin (P < 0.05), tight junction protein 1 (P < 0.01), and claudin 1 (P < 0.05), increased significantly in response to Dex, and expression of defensin beta 1, which can strengthen the innate immune system, was also upregulated (P < 0.05). In addition, BAs increased the expression of the Solute Carrier family 9 member A 2 (P < 0.01) that encodes a sodium hydrogen exchanger. These results suggest that the Dex-induced disruption of BA homeostasis might be mediated through a liver-independent pathway in goats, and the Dex-induced accumulation of TBAs in the cecal digesta may improve volatile fatty acid transportation and mucosal defense.
journal_name
Domest Anim Endocrinoljournal_title
Domestic animal endocrinologyauthors
Hua C,Geng Y,Chen Q,Niu L,Cai L,Tao S,Ni Y,Zhao Rdoi
10.1016/j.domaniend.2018.05.005subject
Has Abstractpub_date
2018-10-01 00:00:00pages
9-16eissn
0739-7240issn
1879-0054pii
S0739-7240(18)30031-6journal_volume
65pub_type
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