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I Yi

Publications and source records attributed to I Yi.

11 recordsLinked to original sources

The effects of food deprivation, nutritive and non-nutritive feeding and wheel running on gastric stress ulcers in rats.

Feeding and housing conditions that induce gastric lesions were investigated. Rats were housed in activity wheels or in hanging cages and exposed to food deprivation, ad lib cellulose or 6 g of cellulose per day for 5 days. Food-deprived rats in both housing conditions had ulcers in the rumen but many rats also had mucosal ulcers. Cellulose prevented rumenal ulcers but produced a tendency toward more severe mucosal ulcers. Ulcers in wheel-housed rats were somewhat larger but the difference was not significant. In a second experiment, rats were fed 6 g/day laboratory chow or 6 g/day chow + ad lib cellulose until b.wt. reached a preset criterion. On the average, about 10 days on the feeding regimen were required to induce ulcers in these groups. None of the rats had rumenal ulcers. Mucosal ulcers were reliably larger in rats that received cellulose in addition to 6 g of chow. There was no difference in ulcer area between wheel-housed and cage-housed rats. The results indicate that solid bulk, regardless of its caloric value or amount, protects the nonglandular stomach whereas noncaloric bulk tends to aggravate ulcers in the glandular stomach. A small amount of chow delays the rate of b.wt. loss and consequently ulcer formation. Furthermore, wheel running is not necessary to produce mucosal ulcers when food intake is insufficient to maintain b.wt. and b.wt. at sacrifice seems to be a good predictor of ulcer formation.

Animals↗

Activity-stress ulcers in rats: the role of preentrainment to meal time.

Rats housed in activity wheels (A-W) or hanging cages (H-C) received food restriction to 4 h/day for 15 days. Food was given at fixed times to entrain the feeding entrainable oscillator or at irregular times to prevent entrainment. One half of the rats received food in the light phase, the other half in the dark phase of the light-dark cycle. Food was then reduced to 6 g/day for 4 days for A-W rats or 7 days for H-C rats. Stomachs were removed 24 h after the last meal and the ulcerated area was quantified. Twenty one of 32 A-W rats and 19 of 32 H-C rats had ulcers in the glandular stomach. Ulcers were significantly larger in A-W rats (p < 0.01). Activity levels (in A-W rats), % body weight loss and terminal body weight (in both groups) were significantly correlated with the area of ulcers. There was no significant time of day effect on the ulcer severity. However, an unexpected finding was that for A-W rats, those fed at fixed times had larger ulcers than those fed at irregular times (p < 0.01) while H-C rats showed an expected trend in the opposite direction. One possible explanation for this result is that for A-W rats, the reduced food supply at an expected time of day generated a greater stress response than in rats whose feeding time was unpredictable.

Animals↗

Stress ulcers in rats: the role of food intake, body weight, and time of day.

Rats were housed in activity wheels (n = 32) or in hanging cages (n = 32) for 2 weeks. Food intake of rats in hanging cages was curtailed to match body weight to that of the activity group. All rats then received 6 g of food at one of four different times of day (n = 8, each mealtime) for 4 consecutive days and were sacrificed 24 h after the last meal. Twenty-three rats in the activity group and 13 rats in the hanging cage group had ulcers in the glandular portion of the stomach. Ulcers were significantly larger and more numerous in the activity group, and activity levels were highly correlated with area of ulceration. In both groups, terminal body weight was also significantly correlated with area of ulceration. No statistically reliable mealtime effects were observed because of large within-group variability. Because many rats in hanging cages developed ulcers in the absence of wheel running, the results suggest that restricted food supply and loss of body weight are initiating factors in ulcer formation, while excessive wheel running contributes to the severity of ulcerations in the glandular stomach.

Animals↗

Body fat reserves attenuate gastric ulcers induced by restricted feeding in rats.

The purpose of this experiment was to explicitly test the hypothesis that the depletion of fat reserves is a critical factor in the generation of ulcers in the glandular stomach. Fat reserves were systematically manipulated by using chow vs. high-fat diets and by using rats of different ages (3, 7, and 17 months). The ulcerogenic procedure consisted of limiting food intake to 6 g of chow per day. For chow-fed rats, 20 days were required to induce ulcers in 3-month-old rats whereas more than 40 days were required in 7- and 17-month-old rats. In 7-month-old rats fed a high-fat diet, the ulcerogenic phase lasted 63 days. Virtually no ulcers were found in control groups with larger body weights that were yoked to the duration of the ulcerogenic phase. Measurement of retroperitoneal and epididymal fat pads indicated that these were nearly depleted in rats with ulcers whereas some fat remained in ulcer-free rats, regardless of age, diet, or the duration of the ulcerogenic phase. These results suggest that the depletion of fat reserves to a critical level triggers a metabolic stress response that then produces gastric ulcers.

Adipose Tissue↗