Fasting induces impairment of gastric mucosal integrity in non‐insulin‐dependent diabetic (db/db) mice

• Published in: Alimentary pharmacology & therapeutics Vol. 14; no. 3; pp. 359 - 366
• Main Authors: KINOSHITA, M, IGARASHI, S, KUME, E, SAITO, N, ARAKAWA, K
• Format: Journal Article
• Language: English
• Published: Oxford UK Blackwell Science Ltd 01.03.2000; Blackwell
• Subjects: Aging; Animals; Associated diseases and complications; Biological and medical sciences; Blood Glucose - metabolism; Body Temperature - physiology; Diabetes Mellitus, Experimental - metabolism; Diabetes Mellitus, Experimental - pathology; Diabetes Mellitus, Type 2 - metabolism; Diabetes Mellitus, Type 2 - pathology; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Fasting - adverse effects; Female; Gastric Mucosa - metabolism; Gastric Mucosa - pathology; Gastroenterology. Liver. Pancreas. Abdomen; Male; Medical sciences; Mice; Mice, Inbred C57BL; Mucins - metabolism; Other diseases. Semiology; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; Time Factors; Endocrinopathy; Stomach; Fasting; Rodentia; Non insulin dependent diabetes; Vertebrata; Mammalia; Mucin; Mouse; Animal; Digestive diseases; Mucosa disease; Gastric disease
• ISSN: 0269-2813; 1365-2036
• DOI: 10.1046/j.1365-2036.2000.00710.x

Background: Although diabetic patients often have gastrointestinal complications, the gastric mucosal function in diabetes has not been well documented. Aim: To investigate the effect of fasting on the gastric mucosa in C57BL/KsJ–db +/+ db (db/db) mice, genetically non‐insulin‐dependent diabetic animals. Methods: Blood glucose levels, gastric mucosal morphology, and the amount of gastric mucin were examined before and after 18 h of fasting with free access to water in db/db mice and their non‐diabetic littermates (db/m). Results: Although 18 h of fasting reduced the blood glucose levels of both db/db and db/m mice, fasting decreased the amount of gastric adherent mucin and caused haemorrhagic gastric lesions only in db/db mice. After fasting, oral administration of ethanol induced much more severe gastric damage in db/db than in db/m mice. The above fasting‐induced gastric damage such as haemorrhagic lesions, loss of the mucin, and the increased sensitivity to ethanol worsened as the duration of diabetes became longer. Glucose ingestion in drinking water during the fasting counteracted the fall in blood glucose and prevented the decrease in the amount of gastric mucin and the formation of gastric mucosal lesions in db/db mice. Conclusion: These findings indicate that fasting‐induced glucose deficit causes gastric mucosal lesions and increases the susceptibility of gastric mucosa to noxious agents owing to the loss of mucus glycoprotein in db/db mice. Prolonged diabetes is likely to augment the severity of fasting‐induced impairment of the gastric mucosal function.