Suppression of enteroendocrine cell glucagon-like peptide (GLP)-1 release by fat-induced small intestinal ketogenesis: a mechanism targeted by Roux-en-Y gastric bypass surgery but not by preoperative very-low-calorie diet.

Objective: Food intake normally stimulates release of satiety and insulin-stimulating intestinal hormones, such as glucagon-like peptide (GLP)-1. This response is blunted in obese insulin resistant subjects, but is rapidly restored following Roux-en-Y gastric bypass (RYGB) surgery. We hypothesised this to be a result of the metabolic changes taking place in the small intestinal mucosa following the anatomical rearrangement after RYGB surgery, and aimed at identifying such mechanisms.

The human duodenal mucosa harbors all components for a local renin angiotensin system.

The renin-angiotensin system (RAS) is present in the gastrointestinal (GI) tract but remains to be fully characterized, particularly in man. The duodenum plays a role in both the upper and lower GI regulation, as well as in distant organs. The present study investigates the presence and functional potential of RAS in the human duodenal mucosa of healthy individuals.

Changes in the mucosa of the Roux-limb after gastric bypass surgery.

Aims: Roux-en-Y gastric bypass surgery is the most efficient treatment of morbid obesity, but the mechanisms of action are still poorly understood. The aim of this study was to explore the Roux-limb mucosa after gastric bypass surgery, focusing upon basic morphology and inflammation.

Methods And Results: Jejunal mucosal samples from the Roux-limb were gathered from eight patients at time of surgery and 6-8 months postsurgery.