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 (65ﾊmg/kg). The experiments were performed using 4-week
STZ-diabetic rats with blood glucose levels above 350ﾊmg/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
Copyrightｩ The Japanese Pharmacological Society 2000
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