Fasting causes gastric mucosal damage in streptozotocin (STZ)-induced diabe
tic rats, but its pathogenic mechanism remains to be elucidated. The aim of
the present study was to investigate the alteration of gastric mucosal muc
in, one of the gastric defensive factors against the development of such da
mage. Diabetes was induced in rats by intravenous injection of STZ (65 mg/k
g). The experiments were performed using 4-week STZ-diabetic rats with bloo
d glucose levels above 350 mg/dl. The amount of gastric mucus glycoprotein
was determined by gel filtration, and the distribution of neutral and acidi
c 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 sig
nificantly 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 diabeti
c rats, the amount of mucus glycoprotein markedly decreased, and both the n
eutral and acidic mucins diminished in the epithelium. Taken together, in S
TZ-diabetic rats, fasting by itself depletes gastric mucus glycoprotein, an
d this depletion may be involved in the pathogenic mechanism of the formati
on of gastric mucosal lesions.