Endocrine Abstracts

Stimulation of insulin release by increased gut hormone levels after gastric bypass surgery, especially glucagonlike polypeptide-1(GLP-1), is considered to be the most important mechanism of action in diabetes remission. However, these beneficial effects can come at a price, namely the development of postprandial hyperinsulinaemic hypoglycaemia, more often called post bariatric hypoglycaemie (PBH). The exact pathophysiology of PBH is not known but GLP-1 plays an important role as blocking the receptor with exendin 9-39 can abolish the occurrence of hypoglycaemia. Altered betacel response, insulin sensitivity, FGF-19, bile acids and the gut microbioma probably also play a role. There is no established definition of PBH as it is probably part of a sliding scale of postprandial glucose values. Consequently, none of the diagnostic tools, self-measured blood glucose, provoking tests like OGTT and MMT, or CGM have established cut-off values. Most authors agree with the diagnosis of PBH in the combination of neuroglycopenic symptoms, a blood glucose level < 2.8 mmol/l with resolution of symptoms with correction of the hypoglycaemia (Whipple’s triad). Treatment of PBH is not supported by well designed studies but relies mainly on clinical experience and case reports. A diet low in carbohydrates is the first step, lowering glucose excursions and thereby diminishing insulin release. Off-label medical treatment is a matter of trial and error and consists of acarbose, reducing postprandial glucose rise, somatostatin analogues, reducing GLP-1 and insulin release, diazoxide, inhibiting insulin secretion or liraglutide, a GLP-1 agonist, the mechanism of action is currently not known. Avexitide, exendin 9-39, a GLP-1r antagonist and colesevelam are promising new medications. Surgical options for PBH, resistant to medication are banding the pouch, placing a feeding tube in the native stomache, an undo operation or even pancreatectomy, all with limited success.