Bariatric surgery induces a new gastric mucosa phenotype with increased functional glucagon-like peptide-1 expressing cells.
Lara Ribeiro-ParentiAnne-Charlotte JarryJean-Baptiste CavinAlexandra WillemetzJohanne Le BeyecAurélie SannierSamira BenaddaAnne-Laure PelletierMuriel HourseauThibaut LégerBastien MorletAnne CouvelardYounes AniniSimon MsikaJean-Pierre MarmuseSévérine LedouxMaude le GallAndré BadoPublished in: Nature communications (2021)
Glucagon-Like Peptide-1 (GLP-1) undergoes rapid inactivation by dipeptidyl peptidase-4 (DPP4) suggesting that target receptors may be activated by locally produced GLP-1. Here we describe GLP-1 positive cells in the rat and human stomach and found these cells co-expressing ghrelin or somatostatin and able to secrete active GLP-1 in the rats. In lean rats, a gastric load of glucose induces a rapid and parallel rise in GLP-1 levels in both the gastric and the portal veins. This rise in portal GLP-1 levels was abrogated in HFD obese rats but restored after vertical sleeve gastrectomy (VSG) surgery. Finally, obese rats and individuals operated on Roux-en-Y gastric bypass and SG display a new gastric mucosa phenotype with hyperplasia of the mucus neck cells concomitant with increased density of GLP-1 positive cells. This report brings to light the contribution of gastric GLP-1 expressing cells that undergo plasticity changes after bariatric surgeries, to circulating GLP-1 levels.
Keyphrases
- induced apoptosis
- cell cycle arrest
- weight loss
- bariatric surgery
- roux en y gastric bypass
- endoplasmic reticulum stress
- type diabetes
- oxidative stress
- endothelial cells
- metabolic syndrome
- signaling pathway
- blood pressure
- minimally invasive
- acute coronary syndrome
- obese patients
- pulmonary embolism
- cell proliferation
- quantum dots
- inferior vena cava