4.8 Article

Dietary α-ketoglutarate alleviates glycinin and β-conglycinin induced damage in the intestine of mirror carp (Cyprinus carpio)

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FRONTIERS IN IMMUNOLOGY
卷 14, 期 -, 页码 -

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FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2023.1140012

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alpha-ketoglutarate; glycinin; beta-conglycinin; intestine immunity; Cyprinus carpio

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This study examined the damage to the intestine caused by glycinin and beta-conglycinin, as well as the alleviating effect of alpha-ketoglutarate. The results showed that intake of soybean protein had negative effects on the growth and immune system of fish, while alpha-ketoglutarate could mitigate the damage.
This study investigated the glycinin and beta-conglycinin induced intestinal damage and alpha-ketoglutarate alleviating the damage of glycinin and beta-conglycinin in intestine. Carp were randomly divided into six dietary groups: containing fish meal (FM) as the protein source, soybean meal (SM), glycinin ( FMG), beta-conglycinin (FMc), glycinin+1.0% alpha-ketoglutarate (AKG) (FMGA), beta-conglycinin +1.0% AKG (FMcA). The intestines were collected on 7(th), and the hepatopancreas and intestines were collected on 56(th). Fish treated with SM and FMc displayed reduced weight gain, specific growth rate, and protein efficiency. On 56(th) day, Fish fed on SM, FMG and FMc presented lower superoxide dismutase (SOD) activities. FMGA and FMcA had higher SOD activity than those fed on the FMG and FMc, respectively. In intestine, fish fed on the SM diets collected on 7(th) presented upregulated the expression of transforming growth factor beta (TGFb1), AMP-activated protein kinase beta (AMPK beta), AMPK gamma, and acetyl-CoA carboxylase (ACC). Fish fed FMG presented upregulated expression of tumor necrosis factor alpha (TNF-alpha), caspase9, and AMPK gamma, while downregulated the expression of claudin7 and AMPK alpha. FMc group presented upregulated expression of TGFb1, caspase3, caspase8, and ACC. Fish fed FMGA showed upregulated expression of TGFb1, claudin3c, claudin7, while downregulating the expression of TNF-alpha and AMPK gamma when compared to fish fed FMG diet. FMcA upregulated the expression of TGFb1, claudin3c than fed on the FMc. In intestine, the villus height and mucosal thickness of the proximal intestine (PI) and the distal intestine (DI) were decreased and crypt depth of the PI and mid intestine (MI) were increased in SM, FMG and FMc. In addition, fish fed on SM, FMG and FMc presented lower citrate synthase (CS), isocitrate dehydrogenase (ICD), alpha-ketoglutarate dehydrogenase complex (alpha-KGDHC) Na+/K+-ATPase activity in DI. FMGA had higher CS, ICD, alpha-KGDHC, and Na+/K+-ATPase activity in PI and MI than those fed on the FMG. FMcA had higher Na+/K+-ATPase activity in MI. In conclusion, dietary soybean meal destroys the intestine's health, the adverse effects are related to the presence of beta-conglycinin and glycinin, especially glycinin. AKG may regulate intestinal energy via tricarboxylic acid cycle, thereby alleviating the damage intestinal morphology caused by the dietary soybean antigen proteins.

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