Sodium butyrate alleviates deoxynivalenol-induced porcine intestinal barrier disruption by promoting mitochondrial homeostasis via PCK2 signaling

文献类型： 外文期刊

第一作者： Xue, Dongfang

作者： Xue, Dongfang;Cheng, Yating;Pang, Tiantian;Kuai, Yunyi;An, Yu;Wu, Kuntan;Li, Yuqing;Lai, Mengyu;Wang, Bihan;Wang, Shuai;Wang, Shuai;Wang, Shuai

作者机构：

关键词： Deoxynivalenol; Sodium butyrate; Mitochondria; Intestinal barrier; Piglets

期刊名称：JOURNAL OF HAZARDOUS MATERIALS （ 影响因子：13.6； 五年影响因子：12.7 ）

ISSN： 0304-3894

年卷期： 2023 年 459 卷

页码：

收录情况： SCI

摘要： Deoxynivalenol (DON) is one of the most plentiful trichothecenes occurring in food and feed, which brings severe health hazards to both animals and humans. This study aims to investigate whether sodium butyrate (NaB) can protect the porcine intestinal barrier from DON exposure through promoting mitochondrial homeostasis. In a 4week feeding experiment, 28 male piglets were allocated according to a 2 by 2 factorial arrangement of treatments with the main factors including supplementation of DON (< 0.8 vs. 4.0 mg/kg) and NaB (0.0 vs. 2 g/kg) in a corn/soybean-based diet. Dietary NaB supplementation mitigated the damaged mitochondrial morphology within the jejunal mucosa and the disrupted gut epithelial tight junctions irritated by DON. In IPEC-J2 cells, we found efficient recovery of the intestinal epithelial barrier occurred following NaB administration. This intestinal barrier reparation was facilitated by NaB-induced PCK2-mediated glyceroneogenesis and restoration of mitochondrial structure and function. In conclusion, we elucidated a mechanism of PCK2-mediated improvement of mitochondrial function by NaB to repair porcine intestinal barrier disruption during chronic DON exposure. Our findings highlight the promise of NaB for use in protecting against DON-induced gut epithelial tight junction disruption in piglets.

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