Effect of vagotomy on gastrointestinal hormones.
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.
D000818:Animals; D002766:Cholecystokinin / Q000378:metabolism; D004285:Dogs; D005749:Gastric Inhibitory Polypeptide / Q000378:metabolism; D005755:Gastrins / Q000097:blood / Q000378:metabolism; D005768:Gastrointestinal Hormones / Q000378:metabolism*; D005934:Glucagon / Q000378:metabolism; D004763:Glucagon-Like Peptides / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D010179:Pancreas / Q000378:metabolism; D010191:Pancreatic Polypeptide / Q000378:metabolism; D010437:Peptic Ulcer / Q000601:surgery*; D012633:Secretin / Q000378:metabolism; D013004:Somatostatin / Q000378:metabolism; D014628:Vagotomy
D005755:Gastrins; D005768:Gastrointestinal Hormones; D007328:Insulin; D012633:Secretin; D013004:Somatostatin; D005749:Gastric Inhibitory Polypeptide; D010191:Pancreatic Polypeptide; D004763:Glucagon-Like Peptides; D005934:Glucagon; D002766:Cholecystokinin