After Roux-en-Y gastric bypass surgery (RYGB, see Figure), changes in the glucose homeostasis are observed. In patients with type 2 diabetes mellitus (T2DM) the glucose homeostasis, insulin resistance and beta cell function improves and in many patients total remission of T2DM is observed. Contrary, 0.5-2% of the patients develops hyperinsulinaemic hypoglycaemia after surgery. The mechanism of diabetes resolution or the development of hypoglycaemia is not completely understood. Most popular theories are the hindgut hypothesis, which states that expedited delivery of nutrients to the distal intestine enhances the secretion of intestinal peptides, such as glucagon-like peptide-1 (GLP-1) and the foregut theory, which states that the exclusion of the proximal intestine food transit results in changes in intestinal peptides.
Furthermore, some suggest a change in beta cells as underlying mechanism of the glucose homeostasis changes. Two animal model studies showed an increase in the number of beta cells after RYGB surgery, additionally in some have shown beta cell hyperplasia in patients with hyperinsulinaemic hypoglycaemia after RYGB surgery. In this project the beta cell mass is visualized in patients before and after RYGB surgery to increase our understanding of the role of the beta cells in T2DM resolution and the development of hyperinsulinaemic hypoglycaemia after RYGB surgery. Visualization will be performed by a Ga68-NODAGA-exendin PET scan. Exendin is a GLP-1 analogue and was shown to bind specifically to beta cells. Radiolabeling with Ga68 makes is possible to measure visualize the beta cell mass in the pancreas non-invasively.