Bile reflux due to disturbed gastric movement is a cause of spontaneous gastric ulcer in W/W-nu mice

c-Kit is a receptor tyrosine kinase, and it is encoded by the mouse W locus . Mutant W/W-v mice develop spontaneous gastric antral ulcers, The aim of t he present study was to investigate the pathogenesis of these gastric ulcer s and to examine the effects of two antiulcer drugs; a proton pump inhibito r (2([4-(3-methoxypropoxy)-3-methylpyridine-2-yl]methyl-sulfinyl)-1H-benzim idazole sodium salt, rabeprazole) and a mucosal protective drug (geranylger anylacetone, GGA), on the gastric ulcers. The inhibition of the gastric aci d secretion by rabeprazole (30 mg/kg body weight, subcutaneous injection on ce a day for six weeks) significantly increased the gastric ulcer formation compared to the controls. In contrast, the GGA treatment (100 mg/kg body w eight, oral administration for six weeks) significantly inhibited the ulcer formation. Bile reflux was seen in these mutant mice, and they showed no c yclic intense contractions in the gastric antrum. These results suggest tha t bile reflux due to the disturbance of gastric antral movement is a cause of the spontaneous gastric ulcers in W/W-v mice.