Acid-induced gastric damage in rats is aggravated by starvation and prevented by several nutrients.
The aggravation of acid-induced gastric damage and its prevention by glucose, ascorbate or glutathione precursors was studied in fed and food-deprived rats. The stomachs of fed rats and those starved for 1, 3 or 5 d were vagotomized just before irrigating for 3 h with solutions containing 0-150 mmol HCI/L. Mucosal glutathione, mucus, lipid peroxides and acid back-diffusion were measured. Stomach ulcers were evaluated by morphological and histological examination. The preventive effects of glucose, ascorbate and a mixture of L-glutamine, L-glycine and L-cysteine were evaluated in the stomachs of rats that were starved for 5 d, vagotomized, then perfused for 3 h with 100 mmol HCI/L. Greater acid back-diffusion and ulcer formation, and lower glutathione and mucus levels in starved rats were dependent on the duration of starvation and luminal acidity. Increased acid back-diffusion and decreased glutathione and mucus production were negatively correlated (r < -0.80, P < 0.05) with ulcer formation. A significant enhancement in mucosal lipid peroxide concentration and serious damage of forestomach and corpus mucosal cells were observed in starved rats exposed to 100 mmol HCI/L. These ulcerogenic factors were effectively inhibited in acid-perfused stomachs of food-deprived rats by daily intraperitoneal injection of the amino acid mixture (150 mg/kg) or by an average daily consumption via drinking water of glucose (10 g) or ascorbate (1.2 g). Starvation aggravated acid-induced gastric damage and was associated with greater acid back-diffusion and oxygen radical generation, and lower mucosal glutathione and mucus production.
Hung
C R
CR
Department of Pharmacology, College of Medicine, National Cheng-Kung University, Taiwan, Republic of China.
Neu
S L
SL
D000596:Amino Acids / Q000008:administration & dosage / Q000627:therapeutic use*; D000818:Animals; D001205:Ascorbic Acid / Q000008:administration & dosage / Q000627:therapeutic use*; D005744:Gastric Acid / Q000502:physiology; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism; D005947:Glucose / Q000008:administration & dosage / Q000627:therapeutic use*; D005978:Glutathione / Q000096:biosynthesis / Q000502:physiology; D006851:Hydrochloric Acid / Q000009:adverse effects* / Q000037:antagonists & inhibitors; D008054:Lipid Peroxides / Q000096:biosynthesis; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013217:Starvation; D013276:Stomach Ulcer / Q000209:etiology* / Q000517:prevention & control; D014628:Vagotomy
D000596:Amino Acids; D008054:Lipid Peroxides; D005978:Glutathione; D005947:Glucose; D001205:Ascorbic Acid; D006851:Hydrochloric Acid