Gastric Intestinal Metaplasia and Bile Acid Dynamics
Summary
Gastric intestinal metaplasia (GIM) represents a critical step in the sequence of alterations that lead from chronic gastritis to gastric cancer. In GIM, the normal gastric epithelium is progressively replaced by cells resembling those of the intestine, reflecting a complex reprogramming of differentiation programmes. Bile acids, normally confined to the duodenum, may reflux into the stomach as a consequence of gastric surgery, motility disorders or pyloric insufficiency. Once present in the gastric lumen, these amphipathic molecules disrupt epithelial integrity, promote chronic inflammation and activate signalling networks that upregulate intestine-specific transcription factors such as CDX2 and KLF4. Bile acid receptors—including the nuclear farnesoid X receptor (FXR) and the membrane-associated G-protein-coupled bile acid receptor (TGR5)—mediate many of these effects, while downstream regulators such as microRNAs and exosomes contribute to epigenetic reprogramming. Converging data also implicate the gut microbiota in modulating bile acid composition and inflammatory tone, further influencing GIM risk. Understanding the interplay between bile acid dynamics and epithelial transformation is essential for developing preventive and therapeutic strategies aimed at interrupting this premalignant process on a global scale.
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Gastric Intestinal Metaplasia and Bile Acid Dynamics publication trend
The graph below shows the total number of articles in gastric intestinal metaplasia and bile acid dynamics across all publications each year (not limited to Nature Index journals).
Technical terms
Gastric intestinal metaplasia (GIM): Replacement of gastric mucosal cells by intestine-type epithelium, considered a precancerous lesion.
Bile acids: Steroid molecules produced in the liver that facilitate fat digestion and act as signalling ligands for nuclear and membrane receptors.
Bile reflux: Retrograde flow of bile into the stomach, leading to mucosal injury and inflammation.
Metaplasia: Reversible phenotypic change in which one differentiated cell type transforms into another under persistent stress.
Mucosoid air-liquid interface model: An in vitro culture technique that exposes epithelial cells to air on one side and nutrient medium on the other, replicating mucosal surface conditions.
References
- Revealing the pathogenesis of gastric intestinal metaplasia based on the mucosoid air-liquid interface. Journal of Translational Medicine (2024).
- Roles and action mechanisms of bile acid-induced gastric intestinal metaplasia: a review. Cell Death Discovery (2022).
- Crosstalk between bile acids and gut microbiota: a potential target for precancerous lesions of gastric cancer. Frontiers in Pharmacology (2025).
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