Evidence for the involvement of secondary bile acids on peripheral and central regulation of feed intake in rainbow trout.

Recent studies suggest that secondary bile acids (SBAs) play a role in energy metabolism and feed intake regulation, but their effects in fish remain largely unknown. This study evaluates the impact of intragastric administration of the main SBAs [500 µM lithocholic acid (LCA), 1,500 µM deoxycholic acid (DCA), and their taurine conjugates: 1,000 µM T-LCA and 600 µM T-DCA] on feed intake, regulatory pathways, and bile acid-related elements in rainbow trout. Results show that all tested SBAs influenced bile acid transporters [apical sodium-dependent bile acid transporter (Asbt), Na+ taurocholate co-transporting polypeptide (Ntcp), organic solute transporter α and β (Ostα, and Ostβ)] and receptors [farnesoid X receptor like-α and β (Fxrα, Fxrβ), and Takeda G protein-coupled receptor 5 (Tgr5)], with DCA and T-DCA mainly affecting the gastrointestinal tract and LCA modulating hypothalamic pathways, suggesting a putative orexigenic role. Plasma analysis confirmed SBA absorption from the gastrointestinal tract into the bloodstream. This study provides the first evidence in fish of SBAs modulating gene and protein expression linked to appetite regulation, underscoring their role in gut-brain communication. Although all SBAs influenced fxr expression, gpbar1 remained unaffected, differing from mammals where BAs suppress appetite. Notably, despite taurine-conjugated SBAs being the most abundant in rainbow trout, only nonconjugated LCA showed significant effects. Taken together, these results provide new information on the emerging importance of SBA in feed intake regulation and bile acid mechanisms.NEW & NOTEWORTHY This study determined for the first time in teleost fish (specifically in rainbow trout): 1) the role of secondary bile acids in the regulation of feed intake and associated signaling pathways, highlighting a putative orexigenic role of lithocholic acid (LCA); 2) the response of Asbt and Ostα transporters and Tgr5 receptor in hypothalamus after LCA administration; and 3) the reabsorption of LCA, DCA, and their taurine conjugates from the gastrointestinal tract into the bloodstream.