Abstract
This study aimed to explore the influence of soybean meal on intestinal mucosa metabolome and signaling pathway of mirror carp (Cyprinus carpio Songpu) by integrating liquid chromatography-tandem mass spectrometry (LC-MS/MS)-based metabolomics. Fish meal (Con) was control group, soybean meal (Dou) group, AMPK activator (300 mg kg–1 Metformin, Met) and AMPK inhibitor (0.2 mg kg–1 Compound-c, c-Com) which added to soybean meal were experimental groups. The metabolome profiles of the intestinal mucosa were determined in fish fed diets Con, Dou, Met, and c-Com on 7th and 59th day. The results were shown: compared with the Con group, the weight gain rate and the specific growth rate of fish experimental groups were significantly decreased (P < 0.05), feed conversion ratio (FCR) was significantly increased (P < 0.05). Compared with the Con group, sphingosine, glycocholic acid, majorities of sugar metabolites were up-regulated, and phosphatidylcholine (PC) and lysophosphatidylcholine (LysoPC), amino acids were reduced significantly in all experiment groups (P < 0.05). Oxidized glutathione was up-regulated in Dou on 7th day, Met on 7th and 59th day (P < 0.05). ADP (adenosine diphosphate) and AMP (adenosine monophpsphate) were up-regulated in Dou, Met, c-Com on 59th day (P < 0.05). Compared with the Dou group, sphingosine was down-regulated on 7th day, up-regulated on 59th day in Met and on 7th and 59th day in c-Com (P < 0.05). Oxidized glutathione and isocitrate on 7th day, L-Valine, L-histidine, and L-isoleucine on 59th day were up-regulated in Met (P < 0.05). Nucleoside metabolites and ADP were up-regulated in c-Com on 7th day (P < 0.05). In conclusion, soybean meal influenced intestinal mucosa metabolic processes, including lipid, amino acid, sugar, apoptosis, and oxidative injury; and changed energy metabolism in intestinal mucosa, enriched in the AMPK, TOR, FoxO signaling pathway; Metformin could aggravate oxidative damage, alleciated apoptosis for the short term, and aggravate apoptosis, improve carbohydrate catabolism and amino acid anabolism for the long term; Compound-c exacerbated apoptosis. repaired oxidative damage, and enhanced nucleoside catabolism.
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