Hyperplasia of the exocrine pancreas after small bowel resection in the rat.

Haegel, P; Stock, C. Chester; Marescaux, Jacques; Petit, B; Grenier, J F

doi:10.1136/gut.22.3.207

Cited by 33 publications

(13 citation statements)

References 28 publications

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“…Associations between changes in the intestine and pancreas have been reported in previous studies. Haegel et al (1981) found that massive resection of the small intestine in rats led to exocrine pancreas hyperplasia. Many studies have addressed the effects of gut hormones on pancreatic hypertrophy and hyperplasia.…”

Section: Discussionmentioning

confidence: 99%

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Pancreatic hyperplasia after gastric bypass surgery in a GK rat model of non-obese type 2 diabetes

Zhou

Qian

et al. 2015

Journal of Endocrinology

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Gastric bypass surgery produces clear antidiabetic effects in a substantial proportion of morbidly obese patients. In view of the recent trend away from 'bariatric' surgery and toward 'metabolic' surgery, it is important to elucidate the enhancing effect of bypass surgery on pancreatic b-cell mass, which is related to diabetes remission in non-obese patients. We investigated the effects of gastric bypass surgery on glycemic control and other pancreatic changes in a spontaneous non-obese type 2 diabetes Goto-Kakizaki rat model. Significant improvements in postprandial hyperglycemia and plasma c-peptide level were observed when glucose was administered orally post-surgery. Other important events observed after surgery were enhanced first phase insulin secretion in a in site pancreatic perfusion experiment, pancreatic hyperplasia, improved islet structure (revealed by immunohistochemical analysis), striking increase in b-cell mass, slight increase in ratio of b-cell area to total pancreas area, and increased number of small islets closely related to exocrine ducts. No notable changes were observed in ratio of b-cell to non-b endocrine cell area, b-cell apoptosis, or b-cell proliferation. These findings demonstrate that gastric bypass surgery in this rat model increases endocrine cells and pancreatic hyperplasia, and reflect the important role of the gastrointestinal system in regulation of metabolism. Key Words" type 2 diabetes mellitus " gastric bypass surgery

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Section: Discussionmentioning

confidence: 99%

“…We measured DNA and protein levels in pancreas, because ratios of DNA and proteins to equivalent volumes of pancreatic tissues are generally indicative of cellular hypertrophy and hyperplasia (Haegel et al 1981). Protein amount per 100 mg pancreas tissue was similar among the three groups (Fig.…”

Section: Effects Of Rygb On Pancreas Hyperplasiamentioning

confidence: 99%

Pancreatic hyperplasia after gastric bypass surgery in a GK rat model of non-obese type 2 diabetes

Zhou

Qian

et al. 2015

Journal of Endocrinology

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“…Clearly this effect could just be an example of non-specific surgically-induced hyperplasia Significance versus control: ** = P <0.001, * = P <0.002. predisposing to carcinogenesis, but the fact that no increase in acidophilic foci was observed after small bowel resection despite a doubling of pancreatic weight is not entirely consistent with this view. The hyperplastic response of the pancreas to a 90% enterectomy is relatively short-lived (Haegel et al, 1981) and may have been inadequate to promote carcinogenesis; others have shown that a minimal threshold level of essential fatty acid in the diet is required to permit tumours to develop in rats given azaserine (Roebuck et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

Pancreatobiliary diversion enhances experimental pancreatic carcinogenesis

Stewart

Flaks²,

Watanapa³

et al. 1991

Br J Cancer

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Summary Since compensatory hyperplasia promotes experimental carcinogenesis in the gut, we tested the ability of two surgical models of pancreatic growth to promote pancreatic carcinogenesis. Male Wistar rats (n = 60) weighing 250 -300 g underwent pancreatobiliary diversion (PBD), 90% small bowel resection (PSBR) or triple transection and reanastomosis of the small intestine (controls). Postoperatively, each group received azaserine (20 mg kg-' wk-' i.p.) for 6 weeks. Surviving rats were killed at 6 months, pancreatic wet weight was measured and histological sections were examined for atypical acinar cell foci (AACF), the putative precursor of carcinoma. Median relative pancreatic weight (mg pancreas/g body weight) was 2.20 for controls (n = 18), 4.08 for PSBR (n = 11) (P <0.001) and 6.86 for PBD (n = 16) (P <0.001). PSBR did not affect the development of acidophilic AACF, but PBD produced an enormous increase in their number per cm3 (median 96 vs 0; P <0.001) and a 7-fold increase in their volume (P <0.001). Both operations cause pancreatic growth, but only PBD promotes carcinogenesis, possibly because of its unique hormonal effect.In the oesophagus, stomach and large intestine, carcinogenesis can be enhanced by luminal factors acting directly on the mucosa, but in the pancreas any such influence (particularly dietary) must be exerted indirectly through hormonal and/or neural connections, i.e. via the enteropancreatic axis. Presumably this type of pathway accounts for the correlation between a high-fat diet and pancreatic cancer mortality (Wynder et al., 1973). In the stomach and colon, hyperplasia precedes and predisposes to neoplasia (Williamson & Rainey, 1984), and the same could be true for the pancreas. Feeding raw soya flour causes hyperplasia of the pancreas in rats and potentiates the carcinogenic effect of azaserine (McGuiness et al., 1981).Pancreatic growth can be stimulated by surgical operations. Thus transposition of a long segment of jejunum to lie between the pylorus and duodenal papilla will cause marked hyperplasia of rat pancreas within 7 days (Stace et al., 1987). This effect may be mediated by an increased secretion of cholecystokinin (CCK) from the jejunum in the absence of pancreatic juice (Miazza et al., 1987). Another surgical stimulus to pancreatic growth in rats is massive (90%) small bowel resection, though here the mechanism is unclear (Stock-Damge et al., 1984): neither CCK nor gastrin appear to be involved.The present study tests the hypothesis that surgical stimulation of pancreatic growth will enhance carcinogenesis. We have used pancreatobiliary diversion and subtotal enterectomy to manipulate the enteropancreatic axis and the formation of acidophilic AACF (atypical acinar cell foci) to indicate early malignant change (Roebuck et al., 1984 tion; the proximal 90% of the jejunoileum was excised with an end-to-end anastomosis between the duodenojejunal flexure and the terminal 5 cm of ileum. The second group (PBD) received pancreatobiliary diversion as previously described (Stace e...

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“…4). Further support for this suggestion is found in the recent report that hyperplasia occurs in the pancreas when 90% of the small bowel is resected (Haegel et al 1981), a procedure which reduced significantly the amount of amylase in the pancreas. The effect of carbachol, both on [6-3H]thymidine incorporation and amylase secretion (Fig.…”

Section: Discussionmentioning

confidence: 79%

“…Quiescent (Go) cells in the exocrine pancreas can be stimulated to divide by a variety of trophic gastrointestinal hormones (Johnson, 1976), by cessation of ethionine treatment (Fitzgerald, Vinijchaikul, Carol & Rosenstock, 1968), by duct ligation (Hultquist, Karlsson & Hallner, 1979), by trypsin inhibitor (Melmed, El-Aaser & Holt, 1976) and by resection of the small bowel (Haegel, Stock, Marescaux, Petit & Grenier, 1981). The role of the autonomic nervous system in th-regulation ofcell division has not been studied in any great detail but has been considered to be less important than hormonal influences (Barrowman, 1975).…”

Section: Introductionmentioning

confidence: 99%

The Effect of Carbachol and Isoprenaline on Cell Division in the Exocrine Pancreas of the Rat

Carling¹,

Templeton²

1982

Exp Physiol

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SUMMARYThe effect of muscarinic cholinergic receptor stimulation on pancreatic acinar cell division has been investigated. Muscarinic receptor stimulation, in addition to causing a 50% depletion of amylase in the pancreas after 4 h, resulted in a 400% increase in the incorporation of [6-3H]thymidine 27 h after drug administration. This increase in incorporation was dosedependent. Autoradiography showed this increase to be due to an increased acinar cell labelling. Isoprenaline also increased the incorporation of [6-3H]thymidine into the pancreas but did not reduce enzyme levels. However, with isoprenaline there was no increase in acinar cell labelling.The possibility of a relationship between secretion and hyperplasia of acinar cells in the rat pancreas is discussed.

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Hyperplasia of the exocrine pancreas after small bowel resection in the rat.

Cited by 33 publications

References 28 publications

Pancreatic hyperplasia after gastric bypass surgery in a GK rat model of non-obese type 2 diabetes

Pancreatic hyperplasia after gastric bypass surgery in a GK rat model of non-obese type 2 diabetes

Pancreatobiliary diversion enhances experimental pancreatic carcinogenesis

The Effect of Carbachol and Isoprenaline on Cell Division in the Exocrine Pancreas of the Rat

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