Effect of Secretin in Functional Dyspepsia and Healthy Subjects
Status:
Completed
Trial end date:
2019-08-01
Target enrollment:
Participant gender:
Summary
Insights into the pathophysiology of functional dyspepsia, with recent demonstration of
inflammation with eosinophilia and mastocytosis in the duodenum (3, 6, 7), providing a
possible lead toward reduced secretion of a potential mediator of post-prandial gastric
accommodation, the gastrointestinal peptide hormone secretin. The dominant site of synthesis
and secretion of this hormone are enteroendocrine S cells in the duodenum.
Inflammation-induced damage to these cells could produce a deficiency. Since intraluminal
acid is a prominent stimulant of S cell secretion, the attempts to treat functional dyspepsia
with anti-secretory medications could actually exacerbate a secretin deficiency syndrome.
This raises the possibility of the therapeutic use of a secretin agonist or a positive
allosteric modulator of the secretin receptor for patients with functional dyspepsia.
Phase:
Phase 1/Phase 2
Details
Lead Sponsor:
Mayo Clinic
Collaborator:
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)