Reactive hypoglycaemia with seizure following intraduodenal glucose infusion in a patient with type 2 diabetes

It was appreciated some 60 years ago that reactive hypoglycaemia may be an ‘early’ manifestation of type 2 diabetes [1]. Postprandial reactive hypoglycaemia is, however, thought to occur rarely in type 2 diabetes; moreover, perhaps only 5 % of those affected exhibit symptoms. Gastric emptying, which exhibits a wide variability (≈1–4 kcal/min) in health, that is even greater in type 2 diabetes is now recognized to be a major determinant of the postprandial glycaemic response, particularly the initial rise in blood glucose [2]. Markedly accelerated gastric emptying of carbohydrate (≈40–100 kcal/min), in the context of altered gastrointestinal anatomy (e.g. Roux-en-Y gastric bypass or RYGB), may cause hypoglycaemia, associated with hyperinsulinaemia, possibly secondary to increased secretion of the incretin hormones (glucose-dependent insulinotropic polypeptide, or GIP, and glucagon-like peptide-1, or GLP-1). In type 2 diabetes, the insulinotropic capacity of GIP is usually markedly diminished [3], and the GLP-1 response is accordingly, central. It is not known whether relatively more rapid emptying from an intact stomach has the capacity to induce an exaggerated GLP-1 response, sufficient to induce severe hypoglycaemia, in type 2 diabetes. usc Refereed/Peer-reviewed