TABLE 1

Medications for managing post–bariatric surgery hypoglycemia: Mechanisms of action

Medication	Mechanism of action
Acarbose^8,23,25,26	Inhibits intestinal alpha-glucosidase—delays absorption of glucose from the intestine, decreases postprandial glycemic and insulinemic peaks
Diazoxide^26–28	Reduces insulin secretion by inhibition of beta-cell adenosine triphosphate–sensitive potassium channels, induces hepatic gluconeogenesis
Octreotide, pasireotide^25,26,29	Somatostatin analogs delay gastric emptying, reduce insulin and GLP-1 secretion
Nifedipine or verapamil^25,30	Inhibits insulin release by inhibiting calcium channels in pancreatic beta cells
GLP-1 analogs^25,26,31	Decreases variability in GLP release, which causes synchronous insulin and glucose peaks, delays gastric emptying, decreases appetite, stimulates glucagon secretion
Dipeptidyl peptidase 4 inhibitors^25,26	Reduces the degradation of GLP-1 and glucose-dependent insulinotropic polypeptide and raises their levels
GLP-1 antagonist^32–34	Prevents surges in GLP-1 and insulin, increases glucagon secretion
SGLT-2 inhibitors^35,36	Reduces carbohydrate absorption by inhibiting intestinal SGLT-1 and increasing hepatic glucose production
Interleukin 1 beta antagonist (anakinra)³⁷	Decreases dysregulated proinflammatory signaling, which can cause excessive insulin response
Glucagon^38,39	Glucagon receptor agonist, stimulates glycogenolysis and hepatic gluconeogenesis
Insulin receptor antibody (XOMA 358)^40,41	Reverses insulin-induced hypoglycemia by significantly decreasing insulin sensitivity and increasing hepatic glucose output

GLP = glucagon-like peptide; SGLT = sodium-glucose cotransporter