Effects of crisp diet on growth, muscle quality, intestine morphology, and gene expression of intestinal-hepatic FXR/PERK pathway in tilapia

Although crispy tilapia is popular in the market, the crisping process can adversely affect its growth and health. To investigate the negative effects of a crisp diet on growth performance, liver and intestinal health of Nile tilapia (Oreochromis niloticus) while improving its muscle quality, tilapia with an initial body mass of (388±35) g were fed either a normal diet (Control group) or a crisp diet (Crisping group) for 120 d. The results showed that compared with the control group, the specific growth rate and condition factor of tilapia in the crisping group decreased significantly, while the feed conversion ratio increased significantly. Muscle hardness, flexibility, hydroxyproline content, and fiber density increased significantly, whereas muscle fiber diameter decreased. In intestinal morphology, villus height increased significantly only in the mid intestinal segment, but decreased in the anterior and posterior intestinal segments. Moreover, varying degrees of degeneration and necrosis of intestinal villus epithelium were observed in all intestinal segments of the crisp group. In intestine, the expression levels of genes related to the inhibition of hepatic bile acid synthesis in the FXR pathway (NR1H4, NR0B2a, FGF19) and those involved in endoplasmic reticulum stress in the PERK pathway (ATF4a, DDIT3) were significantly downregulated in the crisping group. In liver, the expression level of gene related to the inhibition of hepatic bile acid synthesis in the FXR pathway (NR0B2a) was downregulated, while the expression levels of genes involved in bile acid transport in the FXR pathway (NR1H4, ABCB11b) and gene involved in endoplasmic reticulum stress in the PERK pathway (ATF4b) were significantly upregulated. In conclusion, although the crisping diet improves muscle textural properties and hydroxyproline content in Nile tilapia, it reduces growth performance and causes intestinal structural damage. Furthermore, by modulating the expression of genes related to the enterohepatic FXR and PERK pathways, it promotes the synthesis and transport of bile acids in liver and induces mild endoplasmic reticulum stress in liver.