, Volume 49, Issue 3, pp 609-610

Reply to comment on: Patti ME, McMahon G, Mun EC et al. (2005) Severe hypoglycaemia post-gastric bypass requiring partial pancreatectomy: evidence for inappropriate insulin secretion and pancreatic islet hyperplasia. Diabetologia 48:2236–2240

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To the Editor:

We appreciate the interest in our manuscript on hyperinsulinaemic hypoglycaemia post-gastric bypass [1] and the opportunity to respond to the concerns raised by Meier and colleagues [2]. While we hypothesize that excessive secretion of GLP1 may contribute to severe hyperinsulinaemia in the rare cases of post-bypass hypoglycaemia reported in our article [1], we agree it is important to acknowledge that factors other than GLP1 may play a mechanistic role. We also suggested additional potential mechanisms, including improved insulin sensitivity following weight loss unmasking an underlying familial hyperinsulinaemia syndrome, and lack of involution of increased beta cell mass that developed with prior obesity. Furthermore, a descriptive case series of three human patients, for which GLP1 levels are available for only two, makes conclusions regarding the pathogenic role of GLP1 secretion entirely speculative in nature. Markedly high levels of GLP1 in Patients 2 and 3, which p