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Gastrin and the Growth of the Gastrointestinal Tract Gut: First Published As 10.1136/Gut.36.2.203 on 1 February 1995

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Gastrin and the Growth of the Gastrointestinal Tract Gut: First Published As 10.1136/Gut.36.2.203 on 1 February 1995 Gut 1995; 36: 203-208 203 Gastrin and the growth of the gastrointestinal tract Gut: first published as 10.1136/gut.36.2.203 on 1 February 1995. Downloaded from A A Ekundayo, C Y Lee, RA Goodlad Abstract trophic role of gastrin is restricted to While the proliferative effects of gastrin the gastric fundus and the proximal duo- in the gastric fundus are well established, denum. there is a considerable degree of confu- (Gut 1995; 36: 203-208) sion regarding the role of gastrin on the growth of the small intestine and colon. Keywords: cell division, gastrin, growth control. The hypothesis that gastrin is trophic throughout the gut was tested by giving three doses of pentagastrin and one of The gastrointestinal tract is a multilayered gastrin 17 to rats maintained by total defence and absorption system, whose main- parenteral nutrition (TPN). The rats tenance depends on a process of continual cell were fed intravenously for one week, with renewal. Enhanced rates of proliferation are, the various peptides added to the TPN nevertheless, implicated in the pathophysi- diet. The number of vincristine arrested ology of gastrointestinal carcinogenesis and metaphases per gland or crypt was then can act as a promoter of, and can even be con- scored to determine the proliferative sidered to be a cause of carcinogenesis.l Department of state. Both gastrin 17 and pentagastrin Intestinal cell proliferation is controlled by a Histopathology, Royal were found to be trophic in the gastric variety of luminal and systemic influences.2 Postgraduate Medical School, Hammersmith fundus, but not to the gastric antrum. A One gastrointestinal hormone with a well Hospital, London proliferative response was also seen in recorded proliferative role in the stomach is A A Ekundayo the duodenum, but with little evidence of gastrin.A7 Histopathology Unit, a dose response element. No effect on Nevertheless, there is a considerable degree ICRF, London small bowel weight was seen, and no of confusion regarding the role of gastrin on C Y Lee proliferative effect was noted in the mid the growth of the other regions of the gastro- R A Goodlad small bowel, thus the duodenal effect intestinal tract. Johnson8 9 reported that Correspondence to: could be attributed to a local action of gastrin has a general trophic role throughout http://gut.bmj.com/ Dr RA Goodlad, Imperial Cancer Research Fund, increased acid output on the duodenum, the gastrointestinal tract, which led to a spate Histopathology Unit, 35-43 not a general role throughout the small ofpublications challenging this.10 11 12 15 Some Lincoln's Inn Fields, London WC2A 3PN. intestine. No proliferative effects of of the discrepancies in published works could Accepted for publication pentagastrin or gastrin were seen in the be partly attributed to the use of inappropriate 6 May 1994 colon. It is therefore concluded that the techniques to measure cell proliferation, particularly the use of gross tritiated thymidine uptake in mucosal scrapings in vitro.'6 17 Some on September 24, 2021 by guest. Protected copyright. studies using more reasonable methods to 5 study proliferation in hamsters with changed endogenous gastrin concentrations, however, also showed trophic effects on the (fasted) AOVO p < 0.001 T colon.'8 An alternative explanation for these 4 discrepancies is that pentagastrin or gastrin are only trophic to the fasted colon, not to the fed colon.19 20 A role for gastrin in the control of colonic 3 cell renewal has recently been indicated by the finding that gastrin can stimulate the growth of several colon cell lines and a carcinomas.21 X Furthermore, postprandial gastrin concentra- tions may be higher in colon cancer patients,22 2 * T T and recent results show that longlasting endogenous hypergastrinaemia is accom- panied by increased in vivo cell proliferation in the human colonic mucosa. The prevalence of 1 adenomas does not seem to be different in hypergastrinaemia, however, from that of the general population.23 Recent interest in the effects of, and 0L potential risks of, increased gastrin concentra- TPN 65 Rg/ 250 tg/ 1000 Lg/ Gastrin Orally tions has been rekindled by the longterm (control) kg PG kg PG kg PG 17 fed increase in plasma gastrin concentrations Figure 1: The effects ofpentagastrin (PG) and gastrin 17 on gastric pH. AOVO=one way analysis of variance for the TPN control group and the three doses ofpentagastrin. accompanying the introduction, and use * =Significandy different (by t test) to the TPN control group (p<001). of, very effective inhibitors of gastric acid 204 Ekundayo, Lee, Goodlad 0.8 r Stomach 0.5r Caecum T AOVO p = 0.399 I ffi F ,,,.] t 0.4 H- Gut: first published as 10.1136/gut.36.2.203 on 1 February 1995. Downloaded from - 0.8 F ^ i T S//////S_ \\ * T _r mmm//// - WNNNE S/////SS - 3B\\ mm///M/00 - aNNX mm00fimmEM - &MMNNN 0.3 H a/////Smm y0000000S -- &NMNNNm"NNN 0.4 h --3{////// g * M 0.2 H 0.2 H- m - 0.1 H- m//////M_W\\ a///////S_ M\\ IP ._CD m m .5 3 S///////B __ MMMMM\\B Y00000000M _ ssu&&&&Q :0 ..... _ _ 0 0I1 0 0.01 1 .0 4.0 4 Small intestine V&O r, Colon ._ 1= AOVO p = 0-254 l .5) AOVO p = 0.256 t t T 0 CD 0) 3 0.6H T T -T --T 2 0.4 0.2 F- http://gut.bmj.com/ 0.01. - TPN 65 Ag/ 250 ia/ 1000 gl Gastrin Orally TPN 65)g/ 250 jtg/ 1000 ±g/ Gastrin Orally (control) kg PG kg PG kg PG 17 fed (control) kg PG kg PG kg PG 17 fed Figure 2: The effects ofthe various treatments on gastric and intestinal wet Figure 3: The effects ofthe various treatments on caecal and colonic wet weight (expressed as a percentage oftotal body weight). AOVO=one way weight (expressed as a percentage oftotal body weight). AOVO=one way analysis ofvariancefor the TPN control group and the three doses of analysis ofvariancefor the TPN control group and the three doses of pentagastrin. *=Significantly different to the TPN control group pentagastrin. t=significantly different to the TPN control group (p<O O1); t=significantly different to the TPN control group (p<O0OO1). (p<O0OO1). on September 24, 2021 by guest. Protected copyright. secretion. This study was designed to test Saffron Walden, Essex), which is the the hypothesis that gastrin is trophic through- predominant form of gastrin.24 The sixth out the gut, and used the 'starved' gut of the group of rats were orally fed throughout the total parenteral nutrition (TPN) rat, where experiment. the lack of luminal contents, reduced endo- genous secretions, and lowered plasma hormone concentrations should make any ANIMALS effects of exogenous peptides more dis- Male Wistar rats, weighing between 180-200 g cernible. 17 were used. They were housed in rooms with a 14:10 hour light:dark cycle. TPN rats were anaesthetised with 0-06 ml Hypnorm (Janssen Methods Pharmaceuticals, Grove, Oxford) and 0.06 ml diazepam, and a silastic cannula tied into the EXPERIMENTAL DESIGN right external jugular vein. The cannula was Five groups of six rats were infused with tunnelled subcutaneously to the back of the 60 ml/rat/day of a TPN diet for six days. The neck and then taken through a stainless steel first group (control) was infused with the skin button and tether to a fluid swivel joint basic TPN diet. The second group of six (SMA, Barnet, England). The TPN diets were rats were given 65 pug/kg/day of penta- kept at 4°C and pumped into the rats by a gastrin (ICI Pharmaceuticals, Macclesfield, multichannel peristaltic pump, at a rate of Cheshire, England) in the TPN diet. The 60 mI/rat/day giving 1-8 g N, 6.0 g lipid, 8.5 g third and fourth groups of six rats each were glucose, and 1047 kJ per kg per day25 and each given 250 ,ug/kg and 1000 ,ug/kg/day of bag comprised of 2000 ml of the amino acid, pentagastrin respectively. The fifth group was electrolyte, and glucose solution, vamin 9 given 107 ,ug/kg of rat gastrin 17 (Bachem, glucose (KabiVitrum, Uxbridge, Middlesex), Gastrin and the growth of the gastrointestinal tract 205 - Fundus -l AOVOp<0.001 15% SI p = 0.064 t * T T 50h- T rT Gut: first published as 10.1136/gut.36.2.203 on 1 February 1995. Downloaded from 40 -T-- 30 20 10 *0 CDc _ . D U c) L. o U) CDUt0) 0 60r Antrum 0.to 50% SI AOVO 0 |K p.0-923 p=1Oll1 0 (p 0015 * 40 _ AOVO p = 0.193 T -I- 20 _ http://gut.bmj.com/ O L TPN 65 /gl 250 g/ 1000 ugl Gastrin urally TPN 65 utg 250 utg/ 1000 jg/ Gastrin Orally (control) kg PG kg P kg PG 17 fed (control) kg PG kg PG kg PG 17 fed Figure 4: The effects ofthe various treatments on the number ofvincristine Figure 5: The effects ofthe various treatments on the number ofvincristine arrested metaphases per gastric gland. AOVO=one way analysis of arrested metaphases per intestinal crypt. 1 5% SI= 1 5% ofthe length of variancefor the TPN control group and the three doses ofpentagastrin. the small intestine (duodenum) 50% SI=50% ofthe length ofthe small *=Significantly different to the TPN control group (p<0 05); intestine. AOVO=one way analysis ofvariancefor the (TPN control and different to the TPN control group (p<0 01). pentagastrin). *=Significantly different to the TPN control group t=significantly on September 24, 2021 by guest.
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