脆化饲料对罗非鱼生长、肉质、肠道形态及肠-肝FXR/PERK通路基因表达的影响

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

  • 摘要: 脆化罗非鱼虽受市场欢迎,但脆化过程会对鱼的生长和健康产生负面影响。为探究脆化饲料在改善尼罗罗非鱼 (Oreochromis niloticus) 肉质的同时,对生长性能、肝脏和肠道健康产生的负面影响,分别用普通饲料 (对照组) 和脆化饲料 (脆化组) 饲喂体质量为 (388±35) g的尼罗罗非鱼,养殖周期为120 d。实验结果表明:与对照组相比,脆化组尼罗罗非鱼的特定生长率和肥满度均显著降低,饲料系数显著升高;肌肉硬度、弹性等质构特性及羟脯氨酸含量均显著上升,且肌纤维的密度增加、直径减小。脆化组罗非鱼的肠道绒毛高度除中肠段显著升高外,其余肠段均显著降低,且各肠段均伴有不同程度的肠绒毛上皮变性坏死。脆化组肠道FXR通路中抑制肝脏胆汁酸合成的相关基因 (NR1H4NR0B2aFGF19) 与PERK通路中引发内质网应激的相关基因 (ATF4aDDIT3) 的表达量均显著下降;肝脏FXR通路中抑制胆汁酸合成的相关基因NR0B2a的表达量显著下降,而FXR通路中参与胆汁酸转运的相关基因 (NR1H4ABCB11b) 和PERK通路中引发内质网应激的相关基因ATF4b的表达量均显著上升。综上所述,投喂脆化饲料虽提升了尼罗罗非鱼肌肉的质构特性与羟脯氨酸含量,但降低了其生长性能;同时引起肠道结构损伤,并通过影响肠-肝FXR与PERK通路相关基因的表达,促进肝脏胆汁酸的合成与转运,诱发肝脏轻度内质网应激。

     

    Abstract: 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 (crisp group) for 120 d. The results show that compared with the control group, the specific growth rate and condition factor of tilapia in the crisp 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 the 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 crisp group. In the 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 crisp diet improves muscle textural properties and hydroxyproline content in Nile tilapia, it reduces growth performance. It also 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 the liver and induces mild endoplasmic reticulum stress in the liver.

     

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