A 50-year-old woman was admitted to our outpatient clinic for medical workup of a severe form of postprandial hypoglycaemia. Seven years earlier, a Roux-Y gastric bypass was performed due to morbid obesity (preoperative BMI 44.7 kg/m2and weight 129 kg). Within two years, the patient lost 57 kg (BMI 25.5 kg/m2). A year later, the patient noticed, for the first time, hypoglycaemic episodes 1-2 hours after meal intake, which were mainly characterized by loss of concentration, severe fatigue, and auditory and visual impairment that quickly resolved after intake of carbohydrates. An oral glucose tolerance test, at that time, confirmed the presence of symptomatic postprandial hypoglycaemia (2.9 mmol/l). Symptoms persisted despite dietary modifications of up to twelve small meals, each containing a maximum of 20 g of carbohydrates. Off-label treatment with acarbose, saxagliptin, and metformin by her treating physician reduced the frequency and severity of hypoglycaemic episodes but did not significantly improve the situation. Eventually, the patient was referred to our hospital. Her remaining personal history included a mild form of orthostatic dysregulation, migraine, and a multilocular nodular hepatic hyperplasia that required a left-sided hemihepatectomy 17 years ago. The clinical examination was unremarkable apart from irritation-free scars after hemihepatectomy (height, 168 cm; weight, 72 kg; BMI, 25.5 kg/m2; blood pressure, 127/67 mmHg; regular heartbeat, 80 bpm). Laboratory analysis including blood smear; biochemistry comprising electrolytes and kidney and liver parameters; glycated haemoglobin; blood lipids; iron; vitamins B1, B6, B12, and D; and zinc were within reference ranges. A continuous glucose flash monitoring system confirmed a typical pattern of postbariatric hypoglycaemia without any signs of fasting or nocturnal hypoglycaemia. A mixed-meal test (300 ml Ensure plus ) containing 60 g of carbohydrates after a 10-hour fasting period confirmed symptomatic postprandial hypoglycaemia (sweating, drowsiness, odd behaviour, and incoordination) at a glucose level of 2.5 mmol/l, and intravenous glucose administration was required for immediate remission of symptoms (Figure 1(a)). Due to the severe symptomatic presentation of the patient, a 68Ga-DOTA-Exendin-4 PET/CT was performed to exclude an atypical presentation of an insulinoma or focal nesidioblastosis, which might be a surgical target. Therein, the pancreas showed a homogeneous signal distribution (SUV 5.7-8.3), but intensive uptake in the first and second part of the duodenum (SUVmax of 10.0) was observed (Figure 1(b)). To further differentiate this unexpectedly strong tracer accumulation, a double-balloon enteroscopy was performed, which revealed macroscopically unremarkable intraluminal structures in the duodenum. Histologically, there were no signs of malignancy or inflammation (Figure 1(c)). Representative biopsies of the pars 2 duodenii showed normal mucosa with hyperplastic Brunner's glands, which were strongly positive for the GLP-1 receptor on immunohistochemistry but negative for insulin (Figures 1(d) and 1(e)).