Dietary chenodeoxycholic acid inclusion improves carbohydrate utilization and inflammation of largemouth bass (Micropterus salmoides) partly mediated by the activation of farnesoid X receptor.

Abstract

This study evaluated the effects of chenodeoxycholic acid (CDCA), a farnesoid X receptor (FXR) potential activator, on growth performance, antioxidant capacity, glucose metabolism, and inflammation in largemouth bass (Micropterus salmoides) (initial body weight: 5.45 ± 0.02 g) fed a high-carbohydrate diet. Experimental diets included a positive control (5 % α-starch), a negative control (10 % α-starch), and two diets containing 10 % α-starch supplemented with either 0.05 % or 0.10 % CDCA. After 8 weeks, the high-carbohydrate diet reduced growth performance and increased hepatosomatic and viscerosomatic indexes, which were mitigated by 0.10 % CDCA supplementation. The high-carbohydrate diet also increased hepatic glycogen and crude lipid content, both of which were reduced by 0.10 % CDCA. Furthermore, the high-carbohydrate diet induced oxidative stress, histopathological changes, and reduced liver lysozyme activity, which were ameliorated by CDCA supplementation. Molecular analysis showed that the high-carbohydrate diet suppressed FXR and phosphorylated AKT1 (p-AKT1) protein expression in the liver, downregulated insulin signaling (ira, irs, pi3kr1 and akt1), gluconeogenesis (pepck and g6pc), and glycolysis genes (gk, pk and pfkl). CDCA supplementation upregulated fxr expression, activated shp, enhanced the expression of insulin signaling and glycolytic genes (gk, pk and pfkl), and inhibited gluconeogenesis. Additionally, CDCA reduced inflammatory markers (nf-κb and il-1β) and restored anti-inflammatory mediators (il-10, iκb, and tgf-β). In conclusion, 0.10 % CDCA improved carbohydrate metabolism and alleviated liver inflammation in largemouth bass fed a high dietary carbohydrate, partially through FXR activation.