Circulating somatostatin-28 is not a physiologic regulator of gastric acid production in man

Eur J Clin Invest. 1994 Jan;24(1):50-6. doi: 10.1111/j.1365-2362.1994.tb02059.x.

Abstract

Studies were designed to establish the acid inhibitory potency and plasma kinetics of somatostatin-28 (S-28) in humans and to determine whether the amount of S-28 released into the circulation after a meal is sufficient to regulate gastric acid secretion. A liquid meal induced a significant increase of S-28 (P < 0.01) whereas S-14 levels did not change. Postprandial S-28 concentrations were then mimicked by exogenous infusions and tested on basal and pentagastrin-stimulated gastric acid secretion. Expressed in terms of circulating plasma concentrations measured by specific radioimmunoassays, S-14 was 10 times more potent than S-28 in inhibiting gastric acid production. The plasma half-life of S-28 (1.86 min) was longer than that of S-14 (1.00 min) due to a slower plasma clearance rate. S-28 did neither affect basal and stimulated gastric acid secretion nor postprandial intragastric acidity. These studies suggest that postprandial plasma concentrations of S-28 are unlikely to regulate gastric acid secretion in man. They also show that S-28 is several times less potent than S-14 with respect to inhibition of gastric acid output.

Publication types

  • Clinical Trial
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Dose-Response Relationship, Drug
  • Eating / physiology
  • Female
  • Gastric Acid / metabolism*
  • Humans
  • Infusions, Intravenous
  • Kinetics
  • Male
  • Protein Precursors / administration & dosage
  • Protein Precursors / blood
  • Protein Precursors / physiology*
  • Somatostatin / administration & dosage
  • Somatostatin / blood
  • Somatostatin / physiology*
  • Somatostatin-28

Substances

  • Protein Precursors
  • Somatostatin
  • Somatostatin-28