Abstract
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.
Highlights
Among the common gastrointestinal cancers, adenocarcinoma of the pancreas offers a poor prognosis, rivalled only by adenocarcinoma of the gallbladder
The present review examines the hypothesis that hyperplasia and neoplasia are linked in the exocrine pancreas
We have investigated the effects of individual fatty acids on the development of acidophilic acinar cell foci (AACF) (Khoo et al, 1991)
Summary
Like the natural protease inhibitor, camostate markedly increases the development of acidophilic AACF in rat pancreas after azaserine administration, while CR-1409 inhibits the hyperplasia and enhanced neoplasia (Douglas et al, 1989). Similar pancreatic hyperplasia and hypercholecystokininaemia follow camostate feeding in mice (Niederau et al, 1987) and hamsters (Douglas et al, 1990b), but in hamsters CR-1409 treatment does not abrogate this response (Douglas et al, 1990b) Both the natural and synthetic protease inhibitors have somewhat different effects in different species, and CCK displays interspecies variations in its action on the pancreas. Since high-fat diets did not induce pancreatic growth in one rat study (Roebuck et al, 1981b), CCK may not act as a direct tropic influence on the pancreas as it appears to do after administration of trypsin inhibitors. These data are consistent with the finding that dietary protein and CCK work synergistically to stimulate pancreatic growth
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