5:15 p.m. CT Friday, June 12
Gastric bypass surgery (GB) has profound immediate effects on glucose metabolism. The weight-loss independent glycemic effects of GB are attributed to faster passage of ingested glucose into the gut, leading to earlier and higher glycemic peaks followed by lower nadir glucose levels. Along with changes in prandial glucose pattern, meal-induced secretion of insulin and glucagon-like peptide 1 (GLP-1) are also enhanced after GB. Prandial hyperinsulinemia typical of GB is caused by both increased stimulation of beta cells by glucose and GLP-1 and diminished insulin clearance. The glycemic effects of GB are exaggerated in a subgroup of individuals who develop a debilitating condition of postprandial hyperinsulinemic hypoglycemia years after this surgery. Diagnosis of this late complication of GB is complex and requires confirmation of Whipple’s triad. Affected patients have larger systemic appearance of ingested glucose compared to asymptomatic individuals after GB. Hypoglycemia in these patients is also associated with increased glucose clearance as a result of greater GLP-1-induced insulin secretion and lower insulin clearance compared to those without hypoglycemia after this procedure. Here, we discuss the underlying mechanisms as well as the current recommendations regarding diagnosis and treatment of this condition.