Service GJ et al. (2005) Hyperinsulinemic hypoglycemia with nesidioblastosis after gastric-bypass surgery. N Engl J Med 353: 249–254

Gastric-bypass surgery is an increasingly common intervention in the US, where obesity has been described as an epidemic. The procedure has been linked to postprandial symptoms such as dizziness and flushing, which, until recently, have been blamed on the swift emptying of the gastric contents—so-called 'dumping syndrome'. A new report provides an alternative explanation, however; gastric-bypass surgery might lead to the hyperfunction of pancreatic islets, resulting in postprandial hypoglycemia.

Service et al. studied six patients aged 39–54 years who underwent gastric-bypass surgery for obesity. Within 6 months to 8 years of surgery, five of the patients reported episodes of hypoglycemia, occurring 1–3 h after eating. The sixth patient had experienced these symptoms before surgery, but noted that they became more severe afterwards.

Venous blood samples were obtained from the patients during spontaneous episodes, and laboratory analysis confirmed endogenous postprandial hyperinsulinemic hypoglycemia in each case. Selective arterial calcium-stimulation testing pointed to hyperfunction of the pancreatic islets (in one, two, or three arterial distributions), in each case. These findings were used as a basis for partial pancreatectomy in all six patients. All the resected specimens showed evidence of nesidioblastosis; additionally, functional insulinomas were found in one case. During follow-up, the symptoms of postprandial hypoglycemia were reduced in one patient and eliminated in five.

The authors hypothesize that beta-cell trophic factors might be stimulated by gastric-bypass surgery, leading to the observed hypertrophy of the pancreatic islets and the development of hypoglycemia.