title: Studies on hypertrophic effect of 90% partial pancreatectomy on the stomach in rats.
abstract: BACKGROUND
  Stomach changes after major pancreatectomy (Px) are unclear. We previously reported that 90% Px increased stomach weight in rats similarly to endogenous hypergastrinemia by lansoprazole, a proton-pump inhibitor.
  
  
  OBJECTIVE
  To investigate the role of endogenous gastrin in gastric hypertrophy after Px.
  
  
  METHODS
  In male Wistar rats, we compared the wet weight of the stomach and serum gastrin levels between normal (n = 10) or sham-operated controls (n = 10) and 90% partially pancreatectomized rats (n = 7). Then, using Northern blot analysis, we compared gene expression of gastrin, cholecystokinin-B (CCK-B) receptor, and somatostatin in the stomach among normal controls (n = 7), sham-operated rats (n = 7), and 90% partially pancreatectomized rats (n = 8). The samples were obtained on the third and seventh postoperative days (POD).
  
  
  RESULTS
  Wet weight of the stomach was significantly heavier in the Px rats than in the sham-operated controls (3.90 +/- 0.12 mg/g vs 2.63 +/- 0.07mg/g; p< 0.0001) on the 14th POD. Serum gastrin levels were also higher in the Px rats than in controls (161.4 +/- 13.35 pg/mL vs 110.6 +/- 5.67 pg/mL; p< 0.005) on the 14th POD. Gene expression of gastrin in the stomach on the 7th POD was significantly higher in the Px rats than in the sham-operated rats (p < 0.05), and gene expression of CCK-B receptor clearly increased in the Px rats on the 7th POD, when compared with that of controls (p < 0.05). Gastric somatostatin gene expression in both operated groups increased approximately twice as much as in normal controls after operation (p < 0.005). However, on the 7th POD, it returned to control levels only in Px rats and not in sham-operate rats (p < 0.05).
  
  
  CONCLUSIONS
  Increased gene expression of gastrin and CCK-B receptor suggests that gastrin may act as a trophic factor on the stomach after partial Px. Moreover, the relative decrease in gastric somatostatin gene expression may also influence gastric hypertrophy after Px.
authors.affiliation: First Department of Surgery, Shimane Medical University, Izumo, Japan.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Watanabe
authors.forename: Shoichiro
authors.initials: S
authors.lastname: Sumi
authors.forename: Gang
authors.initials: G
authors.lastname: Xu
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Kitamura
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Nio
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Higami
authors.forename: Akihiro
authors.initials: A
authors.lastname: Funakoshi
mesh_terms: D000818:Animals; D015152:Blotting, Northern; D005753:Gastric Mucosa / Q000378:metabolism*; D005755:Gastrins / Q000097:blood / Q000235:genetics; D005786:Gene Expression Regulation; D006984:Hypertrophy; D008297:Male; D009929:Organ Size; D010180:Pancreatectomy; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D043887:Receptor, Cholecystokinin B; D011949:Receptors, Cholecystokinin / Q000235:genetics; D013004:Somatostatin / Q000235:genetics; D013270:Stomach / Q000473:pathology*; D013997:Time Factors
chemical_list: D005755:Gastrins; D012333:RNA, Messenger; D043887:Receptor, Cholecystokinin B; D011949:Receptors, Cholecystokinin; D013004:Somatostatin