Alteration of gastric microbiota and transcriptome in a rat with gastric intestinal metaplasia induced by deoxycholic acid

• DOI: 10.3389/fmicb.2023.1160821
• Publication Date: 2023-05-03T05:03:04Z
• Authors: Zijing Xu; Ling Xiao; Shuaishuai Wang; Yuqin Cheng; Jianping Wu; Yufen Meng; Kaifan Bao; Junfeng Zhang; Chun Cheng
• Keywords: Deoxycholic acid; Taurocholic acid

Objective Bile reflux plays a key role in the development of gastric intestinal metaplasia (GIM), an independent risk factor cancer. Here, we aimed to explore biological mechanism GIM induced by bile rat model. Methods Rats were treated with 2% sodium salicylate and allowed freely drink 20 mmol/L deoxycholate for 12 weeks, was confirmed histopathological analysis. Gastric microbiota profiled according 16S rDNA V3–V4 region, transcriptome sequenced, serum acids (BAs) analyzed targeted metabolomics. Spearman's correlation analysis used constructing network among microbiota, BAs, gene profiles. Real-time polymerase chain reaction (RT-PCR) measured expression levels nine genes transcriptome. Results In stomach, deoxycholic acid (DCA) decreased microbial diversity but promoted abundances several bacterial genera, such as Limosilactobacillus, Burkholderia–Caballeronia–Paraburkholderia , Rikenellaceae RC9 gut group . showed that enriched secretion significantly downregulated, whereas fat digestion absorption obviously upregulated rats. The rats had four namely cholic (CA), DCA, taurocholic acid, taurodeoxycholic acid. Further positively correlated DCA RGD1311575 (capping protein-inhibiting regulator actin dynamics), Fabp1 (fatty acid-binding protein, liver), involved absorption. Finally, Dgat1 (diacylglycerol acyltransferase 1) related identified RT-PCR IHC. Conclusion DCA-induced enhanced function impaired function. DCA– –RGD1311575/Fabp1 axis might play reflux-related GIM.