Bariatric Surgery Induces Gastrin Dependant Proliferation in the Stomach`s Mucosa Specifically in the EC and ECL Cells Population

Bariatric surgery is the definitive treatment for obesity, and has positive effects on DM2 and other metabolic disorders but the mechanism is still unclear.

Gastrin is a gastric hormone that affects the secretion of HCL from the stomach and the proliferation of intestinal mucosa. In sleeve gastrectomy, most of the acid-secreting cells in the stomach are removed, leading to hypergastrinemia and possible changes in the dynamics of gastrin secretion.

In recent studies it was found that after surgery there was an increase in mucosal length (cell proliferation), both in humans and mice, the change was shown to be gastrin dependent using gastrin KO mice.

This proliferation can also be seen through the increased pan-endocrine markers in humans and mice models. And in more extensive research, using single-cell RNA-seq and histology methods it was shown that the only increased endocrine-cell populations are the EC and ECL cells.
Further analysis of the data showed an increase in CCKBR among the ECL population, a Gastrin receptor located on parietal cells and some endocrine cells. This also suggests Gastrin dependency in mediating the mucosal changes after sleeve gastrectomy.

Another marker that was increased in the ECL cell population was PTF1a, a transcription factor important for the development of the pancreas, and other organs. Indeed, factors of the exocrine pancreas are upregulated in ECL cells after surgery.

These findings, and other ongoing research at the lab, indicate that Gastrin is an important factor in the adaptation of the mucosa to the changes after sleeve gastrectomy.