Gut hormone profile and gastric emptying in the dumping syndrome. A hypothesis concerning the pathogenesis

Insulin, enteroglucagon, neurotensin, gastric inhibitory polypeptide (GIP), and motilin have been measured in plasma during an oral glucose test in 76 patients before or after different upper gastrointestinal operations for peptic ulceration. The patients were divided into three clinical groups in accordance with their spontaneous symptoms of dumping after ordinary meals: 26 postoperative patients into a dumping group, 30 postoperative patients into a non-dumping group, and 20 preoperative patients into a reference group. The fasting values of the five hormones were similar in the operated and non-operated groups. Insulin, enteroglucagon, neurotensin, and GIP rose significantly in all patients. The increment of insulin, enteroglucagon, and neurotensin was greater in the postoperative patients with dumping symptoms than in the postoperative and preoperative patients without dumping symptoms. All the patients had a small decrement of motilin. The resulting hypothesis is that an impaired neural control of the gastric emptying is the essential aetiological factor in the dumping syndrome. The excessively rapid delivery of the meal into the jejunum is the abnormal stimulus to the exaggerated hormone release. The response of the small intestine with regard to the hormone release is considered proportionate to the given stimulus. The abrupt fall in circulating blood volume is suggested to play a role in producing the polymorphic symptoms. Neurotensin and GIP cannot be excluded from being the factors arresting the rapid gastric emptying in patients whose neural control has been impaired after gastric surgery.