The role of bile acid in intestinal metaplasia

Abstract

A precancerous lesion of gastric cancer (GC), intestinal metaplasia (IM) is a pathological transformation of non-intestinal epithelium into an intestinal-like mucosa. It greatly raises the risk of developing the intestinal type of GC, which is frequently observed in the stomach and esophagus. It is understood that esophageal adenocarcinoma’s precursor lesion, chronic gastroesophageal reflux disease (GERD), is what causes Barrett’s esophagus (BE), an acquired condition. Recently, Bile acids (BAs), which are one of the compositions of gastric and duodenal contents, have been confirmed that it led to the occurrence and development of BE and gastric intestinal metaplasia (GIM). The objective of the current review is to discuss the mechanism of IM induced by bile acids. This review serves as a foundation for further research aimed at improving the way BE and GIM are currently managed.

Modified Chaishao Liujunzi Decoction inhibits bile acid-induced gastric intestinal metaplasia: from network prediction to experimental verification

“…The EGFR/PI3K/AKT pathway is abnormally activated in the PLGC rat model (including CAG, GIM, and dysplasia), and inhibiting this pathway can effectively improve PLGC [4]. Meanwhile, a key report suggested that BA may promote GIM through the EGFR signaling pathway [9]. Here, our experimental results indicate that DCA can abnormally activate the EGFR/PI3K/AKT/mTOR pathway, promote protein expression of CDX2, MUC2, Ki-67, Cyclin-D1, and induce GIM.…”

“…Chronic inflammation stimulates the gastric mucosa for a long time, which can induce abnormal cell proliferation, AGING promote morphological and functional variations of cells, and then induce GIM or promote the development of GIM toward GC [6][7][8]. Bile reflux is an important factor that triggers or accelerates chronic inflammation [9]. Deoxycholic acid (DCA), as a hydrophobic secondary bile acid (BA), is the main component of bile reflux [10].…”

The role of bile acids in the development of Barrett’s Oesophagus and Oesophageal Adenocarcinoma: a systematic review

“…However, little research has focused on the effects of BAs alone, independent of acidity, on the development of BO and OAC. It is thought that BAs upregulate the expression of metaplasia-promoting genes leading to the columnar-cell phenotype characteristic of BO (49). As GORD progresses to BO, and BO progresses to OAC, the proportion of HCl and secretions in the refluxate decreases dramatically, leaving predominantly BAs (38,50,51).…”

Uncovering the biological mechanism of acupuncture alleviating diabetic nephropathy through homeostasis regulation the of intestinal flora and T lymphocytes

“…In addition, increased urea secretion in the gastrointestinal tract leads to dysbiosis of the intestinal micro ora and disruption of the intestinal epithelial barrier. This leads to reabsorption of ammonia produced by hydrolysis of urea, which accumulates in large quantities in the gastrointestinal tract, via the intestinal mucosa, and resynthesize of urea in the liver, exacerbating renal damage [15].…”