Tirzepatide for refractory post-fundoplication dumping syndrome: A case report

Table 1 Mechanism of action of pharmacotherapies used for dumping syndrome

Pharmacotherapy	Mechanism of action in dumping syndrome
α-glucosidase inhibitor (e.g., acarbose)	Competitively inhibits intestinal α-glucosidases, which delays the breakdown of complex carbohydrates into monosaccharides. This reduces glucose absorption, thereby decreasing postprandial glucose spikes and the subsequent effects of hyperinsulinemia
Uncooked cornstarch	A complex carbohydrate with a low glycemic index that is slowly digested and absorbed offers a gradual release of glucose. This supports maintaining euglycemia and prevents post-meal hypoglycemic episodes
Calcium channel blockers (e.g., nifedipine)	Inhibit voltage-gated calcium channels on pancreatic β-cells, reducing calcium influx inside the cell. This suppresses insulin secretion and helps reduce hyperinsulinemic responses to post-meal glucose elevations
Nondiuretic benzothiadiazine derivative (diazoxide)	Activates ATP-sensitive potassium channels on pancreatic β-cells, causing membrane hyperpolarization. This action inhibits voltage-dependent calcium channels, reducing insulin secretion and countering hyperinsulinemic hypoglycemia
Somatostatin analogues (e.g., octreotide)	Binds to somatostatin receptors, inhibiting insulin secretion and other gastrointestinal hormones like incretins. This decreases postprandial insulin release and slows gastric emptying, thereby preventing hypoglycemia
Avexitide	Glucagon-like peptide receptor (GLP-1) antagonists that reduce postprandial insulin and GLP-1 secretion and increase glucagon

GLP-1: Glucagon-like peptide-1.