Selenium-enriched Lactiplantibacillus plantarum alleviates alkalinity stress-induced selective hepatic insulin...

Carbonate alkalinity is one of the primary factors limiting saline-alkaline water aquaculture, and high alkalinity can lead to respiratory alkalosis, which is hazardous to fish health. Selenium (Se) and Lactiplantibacillus plantarum (L. plantarum) can be used for the biosynthesis of organic selenium (selenium-enriched Lactiplantibacillus plantarum: SL), which has low toxicity, high bioavailability, and the promotion of metabolism. Additionally, it can be used as a feed additive in aquaculture. In the present study, we established a model of chronic alkalinity stress in common carp and added SL to the feed. We found that alkalinity stress can cause severe hepatic dysfunction in common carp, as well as disrupt the intestinal barrier, further contributing to the translocation of enterogenous lipopolysaccharides through portal circulation and exacerbating liver injury. SL alleviated glucose-lipid metabolism abnormalities of the liver while reducing serum LPS levels and reduction of enterogenous LPS translocation to the liver, thus significantly reducing the degree of intestinal villi damage, hepatocyte vacuolisation, and nuclear damage. The significantly increased activities of SOD, GSH-Px, CAT, and T-AOC revealed that SL improved the antioxidant capacity of common carp. SL inhibited the alkalinity stress-induced overexpression of genes related to lipid synthesis and gluconeogenesis by modulating the P13K/Akt/FoxO1 signalling pathway, thus alleviating selective hepatic insulin resistance. SL attenuated the inflammatory response by modulating the mRNA expression levels of IL-7, IL-6, TNF-α and IL-10. In addition, apparent increase in the abundance of pathogenic bacteria (Brevinema, Bosea, Luteolibacter, and Vibrio) and apparent reduction in the abundance of beneficial bacteria (Cetobacterium, ZOR0006, and Shewanella) were closely related to the hepato-intestinal circulation process in carp exposed to alkalinity stress. SL regulated the hepato-intestinal circulation, reduced the abundance of Brevinema, Bosea, Luteolibacter, and Vibrio, increased the abundance of Cetobacterium, ZOR0006, and Shewanella, alleviated alkalinity stress-induced damage to intestinal microvilli (villus height and width), and significantly restored normal liver and intestinal functions. This study reveals the physiological regulatory mechanism by which Se-enriched L. plantarum through liver-intestinal axis alleviates alkalinity stress-induced hepatic insulin resistance and may provide new ideas and a theoretical basis for protecting against alkalosis and treating insulin resistance.