Induction of gastric lesions and hypoglycemic response by food deprivation in streptozotocin-diabetic rats

• Published in: Digestive diseases and sciences 1994-03, Vol.39 (3), p.626-634
• Main Authors: TAKEUCHI, K, UESHIMA, K, OHUCHI, T, OKABE, S
• Format: Article
• Language: English
• Subjects: Animals; Associated diseases and complications; Biological and medical sciences; Blood Glucose - metabolism; Capillary Permeability; Diabetes Mellitus, Experimental - metabolism; Diabetes Mellitus, Experimental - pathology; Diabetes Mellitus, Experimental - physiopathology; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Food Deprivation; Gastric Acid - metabolism; Insulin - pharmacology; Male; Medical sciences; Rats; Rats, Sprague-Dawley; Starvation - pathology; Stomach - pathology
• ISSN: 0163-2116; 1573-2568
• DOI: 10.1007/bf02088352

Overnight fasting causes hemorrhagic lesions in the stomach of streptozotocin (STZ)-induced diabetic rats, but the pathogenetic mechanism remains unknown. The present study was performed to investigate the pathogenesis of such lesions developed in STZ-diabetic rats after starvation, mainly in relation to blood glucose changes. A single injection of STZ (70 mg/kg, intraperitoneally) induced hyperglycemic conditions one week after the administration, and high blood glucose levels (BGL: > 350 mg%) remained up to three weeks later. The STZ-diabetic rats developed gastric lesions with the marked reduction of BGL after 18 hr of fasting, depending upon the duration of diabetes; the lesion score and delta BGL reduction in the 3-week-old STZ rats were 32.0 +/- 7.8 mm and > 250 mg/100 ml, respectively. Acid secretion in the pylorus-ligated rats was not significantly changed in the STZ-induced diabetic conditions for the initial two weeks but slightly decreased at three weeks when compared with normal rats. Fasting of normal rats for 18 hr did not cause either BGL reduction or any lesion in the stomach. In the 3-week-old STZ animals, the severity of gastric lesions increased with the duration of fasting (4-18 hr) and was again closely associated with the degree of delta BGL reduction. These lesions induced by 18 hr of starvation in 3-week-old STZ rats were significantly inhibited by pretreatment with insulin (4 units/rat/day) for the last one week to maintain BGL within normal ranges or by intravenous infusion of 25% glucose during fasting period. Both of these treatments significantly prevented BGL reduction in response to fasting.