The causes for gastric acid hypersecretion remain unexplained inmost patients with duodenal ulcer disease. The present studies represent a continuation of our previous efforts to identify hormonal factors responsible for human gastric hypersecretion. We will concentrate on patients with increased acid secretion but no evidence for gastrinoma. Defects in autoregulation of gastrin release will be sought in ulcer patients by comparison of D50 to exogenous G17 and amount of G17 released in response to peptone at two gastric pH values. Studies will be done to define the nature of antral gastrin cell hyperfunction syndromes. Plasma from patients with acid hypersecretion will be examined for nongastrin stimulants of gastric secretion that could be either immunoglobulins or small molecules. Family studies will be performed to examine the genetics of defects that are identified. The physiology of gastric secretion will be examined by use of the newly developed technique of monoclonal antibody production to develop large amounds of antibodies with defined specificities for gastrin, for gastrin receptors on plasma membranes, and for other peptide stimulants and inhibitors of gastric secretion. These antibodies will be used as blocking agents for hormone action to probe their physiologic roles. Further studies of physiology and structure of bombesin like peptides in human will be done. Finally, efforts will be made to determine the hormonal factors responsible for inhibition of acid secretion during perfusion of the small intestine with fat.
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