Shigeki Igarashi, Eisuke Kume, Hiroshi Narita and Mine Kinoshita
Discovery Research Laboratory, Tanabe Seiyaku Co., Ltd., 2-2-50 Kawagishi, Toda-shi, Saitama 335-8505, Japan
Abstract: Fasting causes gastric mucosal damage in streptozotocin (STZ)-induced diabetic rats, but its pathogenic mechanism remains to be elucidated. The aim of the present study was to investigate the alteration of gastric mucosal mucin, one of the gastric defensive factors against the development of such damage. Diabetes was induced in rats by intravenous injection of STZ (65Ęmg/kg). The experiments were performed using 4-week STZ-diabetic rats with blood glucose levels above 350Ęmg/dl. The amount of gastric mucus glycoprotein was determined by gel filtration, and the distribution of neutral and acidic mucins in the stomach epithelium was examined by histochemical analysis. In normal rats, 24-h fasting neither affected the gastric mucin content nor caused any macroscopic gastric mucosal injury. In contrast, starvation significantly reduced the amount of total gastric mucus glycoprotein prior to the formation of mucosal lesions in the STZ-diabetic rats. Nine hours after food deprivation, the gastric damage developed in about 70% of the diabetic rats, the amount of mucus glycoprotein markedly decreased, and both the neutral and acidic mucins diminished in the epithelium. Taken together, in STZ-diabetic rats, fasting by itself depletes gastric mucus glycoprotein, and this depletion may be involved in the pathogenic mechanism of the formation of gastric mucosal lesions.
Keywords: Fasting, Gastric lesion, Gastric mucus glycoprotein, Streptozotocin-induced diabetic rats
CopyrightŠ The Japanese Pharmacological Society 2000
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