oxyntomodulin and Peptic-Ulcer

Topics: Bicarbonates; Cholecystokinin; Duodenal Ulcer; Gastric Acid; Gastric Inhibitory Polypeptide; Gastrointestinal Hormones; Gastrointestinal Motility; Glucagon-Like Peptides; Humans; Pancreas; Pancreatic Polypeptide; Peptic Ulcer; Secretin; Somatostatin

Different types of vagotomy have been widely used in the treatment of peptic ulcer disease. A close relationship between the vagus nerve and the release or action of gastrointestinal hormones is necessary for the optimal activation of the gastrointestinal tract. The serum concentrations of the antral hormone gastrin are elevated after all types of vagotomy. The postvagotomy hypergastrinemia is due to the change in pH in the antral lumen or the gastric motility changes, both of which may lead to a proliferation of G cells. The reduction in pancreatic secretion after vagotomy is not due to changes in intestinal hormone release, but may be caused by the interruption of a postulated enteropancreatic reflex. Postprandial GIP release and serum insulin levels are not affected by vagotomy, but basal GIP levels are increased after vagotomy. Postprandial pancreatic polypeptide release is nearly abolished by vagotomy, but seems to normalize in the later postoperative course. These findings may be important for the interpretation of pathophysiologic changes after vagotomy.

Topics: Animals; Cholecystokinin; Dogs; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Glucagon-Like Peptides; Humans; Insulin; Insulin Secretion; Pancreas; Pancreatic Polypeptide; Peptic Ulcer; Secretin; Somatostatin; Vagotomy

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.

Topics: Adult; Aged; Dumping Syndrome; Female; Gastric Emptying; Gastric Inhibitory Polypeptide; Gastrointestinal Hormones; Glucagon-Like Peptides; Glucose Tolerance Test; Humans; Insulin; Male; Middle Aged; Motilin; Neurotensin; Peptic Ulcer; Vagotomy

In order to study the pathogenesis of reactive hypoglycemia, the responses of plasma glucose, IRI, glucagon immunoreactivity (GI) and total glucagon-like immunoreactivity (GLI) to 100 g oral glucose load were investigated in twenty-six patients of normal weight with reactive hypoglycemia. Of these patients, nineteen exhibited a diabetic OGTT curve. The findings in these patients were compared to normal control subjects (N = 20) and to disease-matched patients controls (N = 43). The psychological status was assessed by Cornell Medical Index Health Questionnaire in most of the subjects, who also received an x ray examination of the upper gastrointestinal tract. In addition, IVGTT was performed in the hypoglycemic patients. No apparent difference in plasma IRI response to oral glucose was observed between the hypoglycemic patients and their respective controls. Plasma total GLI concentrations were significantly increased during OGTT in both hypoglycemic groups. Following an oral glucose load, plasma GI levels were suppressed in the hypoglycemic groups to an extent similar to that in the control despite an apparent fall in their plasma glucose levels to the hypoglycemic range in the former. Radiological alterations in the upper gastrointestinal tract; deformity of the duodenal cap, gastric and/or duodenal ulcer, were found more frequently in the hypoglycemic groups. However, no characteristic change in personality was noticed in the patients. During IVGTT, neither plasma glucose nor total GLI level of the hypoglycemics differed from that of each control. The pathogenic factors responsible for reactive hypoglycemia will be discussed.

Topics: Glucagon; Glucagon-Like Peptides; Glucose; Glucose Tolerance Test; Humans; Hypoglycemia; Peptic Ulcer