Effect of different concentrations of carbonate on growth performance, intestinal health and hepatic lipid metabolism of Crucian carp

The effects of different concentrations of sodium bicarbonate (0 g/L, 1 g/L, 2 g/L, 3 g/L) on Hefang crucian carp (HCC) were studied. H&E staining, oil red O staining, scanning electron microscopy, transmission electron microscopy, 16S rDNA sequencing, transcriptomic analysis and other techniques were used to observe the pathological changes of intestinal and liver tissues, and detect the changes of intestinal flora and liver gene expression. The main findings are as follows: It was found that the WGR and SGR of the three treatment groups was significantly higher than that of the CK group (p < 0.05). Intestinal H&E staining results showed that the number of goblet cells and the width of submucosa gradually increased with the increase of carbonate concentration. The results of intestinal scanning electron microscopy showed that the roughness of intestinal villi increased slightly with the increase of carbonate concentration. The analysis of populations with large differences among groups treated with sodium bicarbonate of different concentrations found that the relative abundance of Lachnospiraceae varied greatly. LPS levels in the serum, intestinal tract and liver tissue were detected. The results showed that LPS content in MCA and HCA groups was significantly higher than that in CK group (p < 0.05). The expression of claudin 12, 7, c and occludin genes in HCA group and MCA group was significantly lower than that in CK group in intestinal (p < 0.05). The ALT, AST, T-CHO, TG, HDLC, ACC, ACS, CPT-1, HL, LPL and FAS content in HCA group was significantly higher than that in CK group in liver (p < 0.05). The liver was damaged by oil red O staining and transmission electron microscopy. Compared with the control group, the enrichment of steroid biosynthesis is the highest number of DEGs in the HCA group. The iron death pathway and autophagy pathway in HCA group were significantly different from those in CK group (p < 0.05). In summary, this study elucidates that carbonate exposure alters the gut microbiota homeostasis of HCC, leading to intestinal inflammation and increased mucosal barrier permeability, promoting LPS synthesis and absorption, subsequently entering the liver through the gut-liver, increasing liver autophagy and iron death, inducing lipid metabolism disorders, and causing liver injury. In summary, carbonate exposure may cause intestinal microbial disturbance and intestinal injury, and induce liver autophagy and iron death and lipid metabolism disturbance, leading to liver injury