File:PMC5018021 11695 2016 2294 Fig1 HTML.png

English⧼Colon⧽ Fig1: Pathophysiology of dumping syndromes following gastric bypass surgery and mode of action of common therapeutic agents. Reduced gastric volume results in rapid gastric emptying (1) and rapid glucose absorption (2), which induces a hyperinsulinemic response (3), leading to reactive hypoglycemia 1–3 h after food (late dumping syndrome). Rapid delivery of hyperosmolar chyme to the upper small bowel (4) induces release of several vasoactive gut hormones (5), such as vasoactive intestinal peptide, neurotensin, glucagon-like peptide-1 (GLP-1) and glucagon-dependent insulinotropic peptide (GIP), which results in vasomotor symptoms 10–60 min after food (early dumping syndrome). Agents that increase meal viscosity, such as pectin or guar gum, may help to slow down gastric emptying. The α-glucosidase inhibitor, acarbose, can slow down the breakdown and absorption of food sugars. Diazoxide inhibits insulin release from β cells in the pancreatic islets and can attenuate the hyperinsulinemic response. The somatostatin analogue, octreotide, works at multiple levels in the upper gastrointestinal tract, including slowing of gastric emptying and inhibition of secretion and release of insulin and vasoactive gut hormones, and can be useful in the treatment of intractable symptoms of both types of dumping syndrome