Yi I, Stephan F K
Department of Psychology, Florida State University, Tallahassee 32306-1051, USA.
Physiol Behav. 1996 Apr-May;59(4-5):931-6. doi: 10.1016/0031-9384(95)02169-8.
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.
本实验的目的是明确检验脂肪储备耗尽是腺胃溃疡形成的关键因素这一假设。通过使用普通饲料与高脂饮食以及不同年龄(3个月、7个月和17个月)的大鼠,系统地控制脂肪储备。致溃疡程序包括将食物摄入量限制为每天6克普通饲料。对于喂食普通饲料的大鼠,3个月大的大鼠诱导溃疡需要20天,而7个月和17个月大的大鼠则需要40多天。在喂食高脂饮食的7个月大的大鼠中,致溃疡阶段持续63天。与致溃疡阶段时长匹配的体重较大的对照组几乎未发现溃疡。对腹膜后和附睾脂肪垫的测量表明,无论年龄、饮食或致溃疡阶段的时长如何,有溃疡的大鼠这些脂肪垫几乎耗尽,而无溃疡的大鼠仍有一些脂肪。这些结果表明,脂肪储备耗尽至临界水平会引发代谢应激反应,进而导致胃溃疡。