β-conglycinin has been identified as one of the major feed allergens. However, studies of β-conglycinin on fish are scarce. This study investigated the effects of β-conglycinin on the growth, digestive and absorptive ability, inflammatory response, oxidative status and gene expression of juvenile Jian carp (Cyprinus carpio var. Jian) in vivo and their enterocytes in vitro. The results indicated that the specific growth rate (SGR), feed intake, and feed efficiency were reduced by β-conglycinin. In addition, activities of trypsin, chymotrypsin, lipase, creatine kinase, Na+,K+-ATPase and alkaline phosphatase in the intestine showed similar tendencies. The protein content of the hepatopancreas and intestines, and the weight and length of the intestines were all reduced by β-conglycinin. β-conglycinin increased lipid and protein oxidation in the detected tissues and cells. However, β-conglycinin decreased superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione peroxidase (GPx) and glutathione reductase (GR) activities and glutathione (GSH) content in the intestine and enterocytes. Similar antioxidant activity in the hepatopancreas was observed, except for GST. The expression of target of rapamycin (TOR) gene was reduced by β-conglycinin. Furthermore, mRNA levels of interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β) genes were increased by β-conglycinin. However, β-conglycinin increased CuZnSOD, MnSOD, CAT, and GPx1b gene expression. In conclusion, this study indicates that β-conglycinin induces inflammation and oxidation, and causes dysfunction of intestinal digestion and absorption in fish, and finally reduces fish growth. The results of this study provide some information to the mechanism of β-conglycinin-induced negative effects.

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A 60‐day feeding trial was carried out with juvenile Jian carp (Cyprinus carpio var. Jian) to study the effects of myo‐inositol (MI) on the growth, digestive enzyme and intestinal microbial population. Diets with seven levels of inositol (163.5, 232.7, 384.2, 535.8, 687.3, 838.8 and 990.3 mg MI kg−1 diet) were fed to Jian carp (initial weight 22.28±0.07 g). Per cent weight gain (PWG) was improved with increasing inositol levels up to 535.8 mg MI kg−1 diet (P<0.05), and plateaued (P>0.05). The protein production value, lipid production value and ash production value were increased with increasing dietary inositol levels up to 384.2, 838.8 and 838.8 mg MI kg−1 diet respectively (P<0.05). Although intestinal protein content and trypsin activity were not affected by inositol levels (P>0.05), chymotrypsin, lipase and amylase activities in intestine were the lowest for fish fed the MI‐unsupplemented diet (P<0.05). Alkaline phosphatase, Na+, K+‐ATPase, γ‐glutamyl transpeptidase and creatinkinase activities in the intestine were increased with an increase in the inositol levels up to 384.2–687.3 mg MI kg−1 diet (P<0.05). Intestinal Aeromonas hydrophila and Escherichia coli decreased with an increase in the levels of dietary inositol up to 232.7 and 687.3 mg MI kg−1 diet respectively (P<0.05), while Lactobacillus in the intestine increased with an increase in inositol levels up to 990.3 mg MI kg−1 diet (P<0.05). In conclusion, inositol improved growth, digestive capacity and intestinal microbial population of juvenile Jian carp, and the dietary inositol requirement for PWG of juvenile Jian carp is 518.0 mg MI kg−1 diet.

ObjectiveDietary fibre has beneficial effects on energy metabolism, and the majority of studies have focused on short-chain fatty acids produced by gut microbiota. Ginseng has been reported to aid in body weight management, however, its mechanism of action is not yet clear. In this study, we focused on the potential modulating effect of ginseng on gut microbiota, aiming to identify specific strains and their metabolites, especially long-chain fatty acids (LCFA), which mediate the anti-obesity effects of ginseng.DesignDb/db mice were gavaged with ginseng extract (GE) and the effects of GE on gut microbiota were evaluated using 16S rDNA-based high throughput sequencing. To confirm the candidate fatty acids, untargeted metabolomics analyses of the serum and medium samples were performed.ResultsWe demonstrated that GE can induce Enterococcus faecalis, which can produce an unsaturated LCFA, myristoleic acid (MA). Our results indicate that E. faecalis and its metabolite MA can reduce adiposity by brown adipose tissue (BAT) activation and beige fat formation. In addition, the gene of E. faecalis encoding Acyl-CoA thioesterases (ACOTs) exhibited the biosynthetic potential to synthesise MA, as knockdown (KD) of the ACOT gene by CRISPR-dCas9 significantly reduced MA production. Furthermore, exogenous treatment with KD E. faecalis could not reproduce the beneficial effects of wild type E. faecalis, which work by augmenting the circulating MA levels.ConclusionsOur results demonstrated that the gut microbiota-LCFA-BAT axis plays an important role in host metabolism, which may provide a strategic advantage for the next generation of anti-obesity drug development.

Spatial cognitive impairment is common after stroke insults. Voluntary exercise could improve the impaired spatial memory. Newly generated neurons in the dentate gyrus are necessary for the acquisition of new hippocampus-dependent memories. However, it is not well known whether voluntary exercise after stroke promotes neurogenesis in the adult dentate gyrus, thereby promoting spatial memory recovery. Here, we examined in mice subjected to focal cerebral ischemia the effect of voluntary or forced exercise on neurogenesis in the ischemic dentate gyrus and spatial memory. Exposure to voluntary wheel running after stroke enhanced newborn cell survival and up-regulated the phosphorylation of cAMP response element binding protein (CREB) in the dentate gyrus and reversed ischemia-induced spatial memory impairment. However, the enhanced newborn cell survival and CREB phosphorylation in the dentate gyrus and improved spatial memory were not observed in the mice exposed to forced swimming. Moreover, there was a significant correlation between the total number of surviving newborn cells in the dentate gyrus and the ability of mice to locate the platform in the Morris water maze. These results suggest that, in the adult mice, exposure to voluntary exercise after ischemic stroke may promote newborn cells survival in the dentate gyrus by up-regulating CREB phosphorylation and consequently restore impaired hippocampus-dependent memory.

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This study was designed to determine the dietary lysine requirement of juvenile Jian carp (cyprinus carpio var. Jian). A total of 990 juvenile Jian carps (initial weight 7.89 ± 0.04 g) were randomly allocated six groups of each three replicates, feeding isonitrogenous (320 g kg )1 crude protein) and isolipidic (50 g kg )1 crude fat) diets containing graded levels of coated L L-lysine, with dietary lysine content ranging from 22 to 69 g kg )1 of protein, respectively, for 80 days. Final weight, protein deposition and protein production value were significantly improved in response to the increasing levels of dietary lysine up to 59 g kg )1 of protein and remained nearly constant thereafter. Whole-body protein content followed a similar pattern as growth parameters in relation to dietary lysine level. Hepatopancreas and intestine protein content, hepatopancreas index (HSI) and intestine index (ISI) were positively affected by dietary lysine level. The dietary lysine requirement of juvenile Jian carp estimated by broken line analysis based on weight gain was 59 g kg )1 of protein. KEY WORDS