The Effect of Somatostatin on Postresectional Ileal Hyperplasia

Abstract

After somatostatin infusion in rats, the proliferative activity in ileal crypts was examined under a variety of circumstances known to influence mucosal behaviour. The anticipated hyperplastic response to resection was inhibited by somatostatin treatment, not only under conditions of intestinal continuity but also in isolated segments of ileum. These results suggest that postresectional ileal hyperplasia is humorally mediated and is explicable on the basis of somatostatin suppression of trophic gut hormones. However, a direct effect of somatostatin and other secondary effects cannot be excluded.

Towards Understanding the Process of Intestinal Adaptation

“…vasoactive intestinal polypeptide, bombe sin. and pancreatic peptide remain to be eluci dated [39], In addition, a few studies indicate that somatostatin might have an inhibiting role in the adaptation process while prosta glandin and testosterone might play an augmentory role [40][41][42][43]. It is likely that all the humoral signals discussed function in concert with neurovascular effects.…”

Epidermal Growth Factor Inhibits Somatostatin-Induced Apoptosis

“…Somatostatin and its analogue octreotide inhibit the regenerative response to intestinal injury and the adaptive response to intestinal resection [1][2][3]. These effects are due not only to a reduction in enterocyte migration and proliferation but also to a stimulated rate of apoptosis, or programmed cell death, in both crypt and villus enterocytes [4].…”

Short Bowel Syndrome: Intestinal Adaptation and Medical Therapy

“…Unfortunately, che effect of somatostatin analogues appears to be only transient ( 127). Furthermore, a study by Holmes (128) Short bowel syndrome: Medical therapy plastic response co ileal resection and inhibits nutrient absorption. For these reasons, somatostatin has limited use in short bowel syndrome at present.…”