Effects of Somatostatin on Gastrointestinal Propagation and Absorption of Oral Glucose in Man

Abstract

The effects of i.v. somatostatin, 6.0–0.05 μg · min^-1, on the gastric emptying and on the transit times and glucose absorption in the proximal 70 cm of the small bowel after 75 g of oral glucose were examined in healthy subjects with a multiple-marker dilution method. In the controls the stomach emptied the hypertonic glucose solution in 3 h and 48 ± 4 g of glucose was absorbed in the intestinal test segment. Approximately even proportions were absorbed from the emptied glucose portions throughout the experiments; variations were caused by the varying transit time, the absorption being more complete the longer the time to transit the segment. Somatostatin, started 20 min before oral glucose and infused for 1 or 2 h, prolonged dose-dependently the transit time. A maximal prolongation from 15 ± 2 min in the controls to 55 ± 7 min (p < 0.01) was attained by 0.5 μg · min^-1, and 0.05 μg · min^-1 somatostatin gave a significant twofold slowing. The inhibition of the intestinal motility persisted in the postinfusion period and was followed by a late sudden acceleration of the propagation speed. The gastric emptying rate was reduced by somatostatin, but the inhibition was slowly established and of marginal consequences for the absorption. 2-Hour infusions of more than 1.5 μg · min^-1 delayed the complete emptying. Somatostatin reduced dose-dependently the glucose absorption rate in the segment. In the controls the absorption rate of 9.5 ± 1.4% · min^-1 of transit decreased to 4.2 ± 0.7% min^-1 (p < 0.02) after a dose of 0.05 μg· min^-1 and to 2.6 ± 0.1 % · min^-1 (p < 0.01) after 0.5 μg · min^-1 of somatostatin and was further lowered by higher doses. The lower effectiveness was compensated by the prolonged transit times so that the totally absorbed glucose in the segment approached the control value. An absolute reduction was only recorded in early phases of the experiments before the transit was slowed and it seems to result in spite of prolonged transit from infusion rates of 1.5 μg · min^-1 or more somatostatin. Dose-related side effects from the digestive tract and due to hypoglycemia in the late postinfusion period were common with infusion rates exceeding 0.5 μg · min^-1. The study shows that exogenous somatostatin delays and evens out the uptake of oral glucose in the proximal small bowel by dose-dependent inhibitory effects on the gastrointestinal motility and reductions of the glucose absorption rate. The effects could be produced by somatostatin doses a hundred times lower than previously tested for effects in the human gastrointestinal tract.