Tropic role of enteroglucagon in pancreatic adaptation to subtotal enterectomy

Proximal small bowel resection causes pancreatic hyperplasia, presumably via a humoral mechanism. Although cholecystokinin can stimulate pancreatic growth, its proximal distribution in the gut makes it an unlikely intermediary after proximal small bowel resection. The potential roles of neurotensin and enteroglucagon were studied, since these hormones are mainly secreted from the ileum and proximal colon. Male Wistar rats (n = 50) weighing 200–250 g were randomized to receive 90 per cent proximal small bowel resection or jejunal transection and resuture (control). Rats were killed at 1 week or 1 month, when plasma was obtained for hormone assay and the pancreas was excised for protein and nucleic acid measurement. Proximal small bowel resection increased circulating enteroglucagon levels by 150 per cent at 1 week (P < 0.002) and by 83 per cent at 1 month (P < 0.005); neurotensin levels were unchanged. Pancreatic wet weight was 21 per cent greater 1 month after proximal small bowel resection (P < 0.001). Proximal small bowel resection increased protein, RNA and DNA contents of the pancreas both at 1 week and at 1 month. Since plasma enteroglucagon correlated with these indices of pancreatic mass, enteroglucagon may have a pancreatotropic role (in addition to its enterotropic role).