Enhancement of small intestine function by gastrin

Abstract

Frequently, congenital or acquired small intestine (SI) abnormalities in infants lead to inadequate absorption. Gastrin has been suggested as a trophic hormone for SI epithelial cells. We chose to evaluate the effect of gastrin on the function and maturation of developing SI using a rat fetal intestine transplant model. Jejunoileal segments (7–8 cm) obtained from 19 to 20 days gestation fetal rats were implanted subcutaneously in syngeneic adult rats. Two weeks following transplantation the control group ( N = 10) was continuously infused with saline and the study group ( N = 9) was continuously infused with gastrin-17 (13.5 n M/kg/day) for 14 days. Following the infusion, intestinal maturation and function were evaluated by mucosal DNA concentration, disaccharidase activity, and absorption of [ 14C]galactose and [ 14C]glycine. Absorption (μ M/cm 2 SI) by the control and study groups for galactose was 1.10 ± 0.18 vs 2.73 ± 0.25, and for glycine was 1.68 ± 0.23 vs 2.22 ± 0.26, respectively. DNA concentration (μg/mg SI) of the control and study groups was 410 ± 43 vs 1031 ± 158, respectively. Lactase and sucrase activity were similar in both groups. Although maltase (μ M substrate hydrolized/min/g SI) was 13.5 ± 2.7 for the gastrin group vs 7.9 ± .9 for the control group, statistical significance was not achieved. Thus, gastrin produced a statistically significant increase in DNA concentration (cell mass) ( P < 0.01). More importantly, to our knowledge, this is the first demonstration that exogenously administered gastrin can increase absorption of carbohydrate (galactose; P < 0.01) and protein (glycine; P < 0.05). We conclude that further studies on the trophic effects of gastrin are indicated to determine if they have a therapeutic role in patients with short bowel syndrome.