Pancreatic Hyperplasia after Small Bowel Resection in the Rat: Dissociation from Endogenous Gastrin Levels

Abstract

Extensive small bowel resection produces pancreatic hyperplasia and increases plasma gastrin levels in the rat. Because gastrin is known as a trophic factor for the exocrine pancreas, we studied the effect of endogenous variations of gastrin induced by different gastric operations on the rat pancreas in both resected and transected animals. Vagotomy increased plasma gastrin level while antrectomy decreased it; pyloroplasty was without any effect. These gastric operations enhanced slightly but not significantly the pancreatic weight, its protein and DNA content. A 90% jejunoileal resection alone increased markedly these parameters while mitotic figures appeared in acinar cells. Pyloroplasty, vagotomy and antrectomy did not modify the changes induced by intestinal resection itself except the level of protein. These findings suggest that hypergastrinemia produced by intestinal resection is not responsible for pancreatic hyperplasia.

Adaptive Changes in Rat Exocrine Pancreas following Subtotal Colectomy

“…Pancreatic hyperplasia, not hypertrophy, was shown to develop in rats after subtotal [20] or distal small-bowel resection [3] both in the presence and absence of hypergastrinemia [20]. We obtained similar results of pancreatic growth following distal smallbowel resection [14], In rats, therefore, the distal small bowel seems to contain inhibitory factors, too.…”

Indication for pancreatic enzyme substitution following small intestinal resection (short bowel syndrome)

“…The conclusion that the secretory capacity of the pancreas and its response to physiological stimuli may not be altered by the syndrome is supported by experimental studies in rats in which even hypersecretion and pancreatic hyperplasia have been observed [5,31]. On the other hand, a decreased duodenal activity of pancreatic enzymes in rats after small intestine resection suggesting pancreatic dysfunction was reported by Murillo et al [22] and Carreras et al [1].…”

Adaptive Changes of the Exocrine Pancreas and Plasma Cholecystokinin Release following Subtotal Gastric Resection in Rats

“…Dembinski and Johnson [9] performed antrec tomy combined with exogenous administra tion of gastrin and provided further evi dence for gastrin as a trophic factor for the pancreas. However, in the studies of Oscarson et al [10], who showed adaptive pan creatic changes after BII gastrectomy, and in studies of Stock Damge et al [11], who found a trophic effect following subtotal small intestinal resection persisting after an trectomy, the trophic effect of gastrin was questioned. In our experiments, the reduc tion of gastrin-producing cells by distal gas tric resection supports the latter theory that gastrin does not play a major role in pan creatic trophism.…”

“…Evidence for gastrin as a trophic agent is given using an experi mental rat model [8,9], whereas this finding is not confirmed in other experiments [10,11].…”