Effects of dietary enzymatically treated Artemisia annua L. in low fish meal diet on growth, antioxidation, metabolism and intestinal health of Micropterus salmoides

The excessive substitution of fish meal (FM) by Clostridium autoethanogenum protein (CAP) could reduce the growth performance and disrupt the intestinal structural integrity of Micropterus salmoides. In order to solve this problem, an eight-week feeding trial was conducted to investigate the effects of dietary enzymatically treated Artemisia annua L. (EA) in low FM diet containing high-CAP on growth, antioxidation capacity, lipid and car-bohydrate metabolism and intestinal microbiota of M. salmoides. Six isonitrogenous and isolipid experimental diets were produced containing 0 g/kg, 0.25 g/kg, 0.5 g/kg, 1.0 g/kg, 2.0 g/kg and 4.0 g/kg of dietary EA, which were named EA0, EA0.25, EA0.5, EA1.0, EA2.0 and EA4.0, respectively. After the feeding trial, the weight gain rate (WGR) and specific growth rate (SGR) were significantly increased in EA0.25, EA0.5 and EA 1.0 groups compared to EA0 group. The digestive enzyme activities in stomach and intestine, and the villus width and muscular layer thickness of the intestine were increased by dietary EA. Dietary EA improved the antioxidation capacity and serum lipid level of M. salmoides. The expression levels of sterol regulatory element-binding protein 1-c (srebp1-c), acetyl-coa carboxylase alpha (acc alpha), fatty acid synthase (fan), 3-hydroxy-3-methylglutaryl-coa reductase (hmgcr) and acc beta were significantly upregulated by 4.0 g/kg of dietary EA. The mRNA level of peroxisome proliferator-activated receptor alpha (ppar alpha) and carnitine palmitoyltransferase 1 (cpt-1) were upregulated by 4.0 g/ kg and 0.5 g/kg of dietary EA, respectively. Besides, the glucose content in serum was decreased by EA. The expressions of forkhead box o1 (foxo1), phosphoenolpyruvate carboxykinase (pepck), fructose bisphosphatase (fbp), glucokinase (gk) and pyruvate kinase (pk) were significantly improved by 4.0 g/kg of dietary EA, and the level of phosphofructokinase (pfk) was upregulated by 0.5 g/kg of dietary EA. The addition of 0.5 g/kg of dietary EA could optimize beneficial Cetobacterium and reduce harmful Mycoplasmataceae abundances in intestine of M. salmoides. In summary, the appropriate amount of dietary EA could be added to the high-CAP diet to improve the growth performance, antioxidation, lipid and carbohydrate metabolism, liver and intestinal health of M. salmoides. This study will provide scientific guidance for replacing FM with non-food proteins.