Duodenogastric reflux enhances growth and carcinogenesis in the rat pancreas

Watanapa, P.; Flaks, Bojan; Oztast, H.; Deprez, Pierre Henri; Calam, J.; Williamson, R. C. N.

doi:10.1002/bjs.1800790827

Cited by 21 publications

(7 citation statements)

References 23 publications

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“…Nevertheless, infusion of harvested pancreaticobiliary secretions into isolated intestinal loops shows that these secretions do themselves have a direct trophic action to the mucosa. 1 We agree that the effects of a circulating hormone alone cannot account for the changes seen in jejunoileal transposition, where the transposed ileum undergoes hyperplasia and the transposed jejunum hypoplasia. 2 The direct effects of luminal nutrients may, however, be relevant to these changes.…”

supporting

confidence: 51%

Duodenogastric reflux and pancreatic growth.

Williamson¹,

Watanapa²

1995

Gut

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supporting

confidence: 51%

Duodenogastric reflux and pancreatic growth.

Williamson¹,

Watanapa²

1995

Gut

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“…We have further investigated the effect of duodenogastric reflux on pancreatic growth and chemical carcinogenesis. Six months after split gastrojejunostomy rats had greater pancreatic weight, and only those with duodenogastric efflux showed any preneoplastic foci after azaserine treatment (Watanapa et al, 1992c). On this occasion plasma CCK levels were unchanged, while both basal and postprandial plasma gastrin levels were increased by split gastrojejunostomy.…”

Section: Other Specific Dietary Constituentsmentioning

confidence: 73%

Experimental pancreatic hyperplasia and neoplasia: effects of dietary and surgical manipulation

Watanapa

Williamson²

1993

Br J Cancer

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Summary Several studies carried out during the past two decades have investigated the effect of dietary and surgical manipulation on pancreatic growth and carcinogenesis. Diets high in trypsin inhibitor stimulate pancreatic growth and increase the formation of preneoplastic lesions and carcinomas in the rat pancreas. Cholecystokinin (CCK) is the key intermediary in this response, since both natural and synthetic trypsin inhibitors increase circulating levels of the hormone and CCK antagonists largely prevent these changes. Fatty acids enhance pancreatic carcinogenesis in both rats and hamsters, whereas protein appears to have a protective role in the rat, but to increase tumour yields in the hamster. Several surgical operations affect the pancreas. Pancreatobiliary diversion and partial gastrectomy stimulate pancreatic growth and enhance carcinogenesis, probably by means of increased CCK release. Complete duodenogastric reflux has similar effects on the pancreas but the gut peptide involved is gastrin. Although massive small bowel resection increases pancreatic growth, the marked reduction in caloric absorption probably explains its failure to enhance carcinogenesis. CCK and enteroglucagon might work in concert to modulate the tropic response of the pancreas to small bowel resection. In the pancreas, as in the large intestine, hyperplasia appears to precede and predispose to neoplasia.

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“…With regard to the effects of gastrin on experimental pancreatic carcinogenesis, data are very limited.29 45 Previous studies showed that gastric fundectomy or split gastrojejunostomy with hypergastrinaemia enhanced azaserine induced pancreatic carcinogenesis in the rat. 29 45 In the present study, however, fundectomy did not significantly influence the incidence or labelling index of pancreatic lesions, indicating that early preneoplastic pancreatic lesions in the hamster are not sensitive to endogenous gastrin.…”

Section: Discussionmentioning

confidence: 99%

Effect of chronic endogenous hypergastrinaemia on pancreatic growth and carcinogenesis in the hamster.

Chu

Kullman

Rehfeld

et al. 1997

Gut

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Background-To examine the effect of gastrin on spontaneous and induced pancreatic carcinogenesis in the hamster. Methods and results-Two sets of experiments were carried out, one involving long term hypergastrinaemia and one involving cancer induction during hypergastrinaemia. The effect of hypergastrinaemia accomplished by gastric fundectomy was studied for eight months. Neither fundectomised hamsters nor sham operated controls developed premalignant or malignant pancreatic lesions. In the fundectomy group, the mean pancreatic weight, total protein content, and DNA content was increased by 28%, 25%, and 25% respectively. No such increases were found in fundectomised animals receiving a cholecystokinin-B receptor antagonist during the last 24 days of the experiment. In the cancer induction study, the effect of fundectomy on N-nitrosobis(2-oxopropyl)amine induced pancreatic carcinogenesis was studied for three months. There were no significant differences in the incidence or ['H]-thymidine labelling index of focal pancreatic lesions between fundectomised and sham operated control animals.Conclusions-Fundectomy with chronic hypergastrinaemia induces pancreatic hypertrophy, but does not enhance Nnitrosobis(2-oxopropyl)amine induced pancreatic carcinogenesis in the hamster. The increases in growth were inhibited by a cholecystokinin-B receptor antagonist, indicating that the trophic effect of fundectomy is mediated by gastrin. (Gut 1997; 40: 536-540)

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Duodenogastric reflux enhances growth and carcinogenesis in the rat pancreas

Cited by 21 publications

References 23 publications

Duodenogastric reflux and pancreatic growth.

Duodenogastric reflux and pancreatic growth.

Experimental pancreatic hyperplasia and neoplasia: effects of dietary and surgical manipulation

Effect of chronic endogenous hypergastrinaemia on pancreatic growth and carcinogenesis in the hamster.

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