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. 2003 Mar;26(2):e43-7.
doi: 10.1097/00006676-200303000-00025.

Studies on hypertrophic effect of 90% partial pancreatectomy on the stomach in rats

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Studies on hypertrophic effect of 90% partial pancreatectomy on the stomach in rats

Hiroaki Watanabe et al. Pancreas. 2003 Mar.

Abstract

Introduction: 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.

Aim: To investigate the role of endogenous gastrin in gastric hypertrophy after Px.

Methodology: 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).

Conclusion: 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.

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