Simanowski U A, Seitz H K, Baier B, Kommerell B, Schmidt-Gayk H, Wright N A
Gut. 1986 Mar;27(3):278-82. doi: 10.1136/gut.27.3.278.
Cell proliferation was examined in the gastrointestinal tract of 30 pair fed rats having received an isocaloric liquid diet containing 36% of total calories either as ethanol or carbohydrates for four weeks. Utilising the metaphase arrest technique with vincristine, cell proliferation was measured as crypt cell production rate. This was selectively increased in the rectal mucosa of ethanol fed rats (19.1 +/- 2.0 vs 9.1 +/- 1.8 cells/crypt/h; p less than 0.005). There was a concomitant increase in proliferative compartment size (48.1 +/- 5.6% vs 30.1 +/- 8.5% of crypt population size; p less than 0.001). Serum gastrin concentrations were also found to be significantly increased after ethanol feeding (172 +/- 51 vs 106 +/- 27 pmol/l; p less than 0.01). The ethanol dependent proliferative changes in the rectal mucosa are predictive of higher susceptibility of this site to carcinogenesis, supporting experimental and epidemiological data. Increased gastrin concentrations may partly explain the observed rectal hyperproliferation. Other possible causes cannot, however, be excluded.
在30只成对喂养的大鼠的胃肠道中检测细胞增殖情况,这些大鼠接受了一种等热量的液体饮食,其中总热量的36%要么来自乙醇,要么来自碳水化合物,持续四周。利用长春新碱的中期阻断技术,细胞增殖以隐窝细胞产生率来衡量。在喂食乙醇的大鼠的直肠黏膜中,隐窝细胞产生率有选择性地增加(19.1±2.0对9.1±1.8个细胞/隐窝/小时;p<0.005)。增殖区大小也随之增加(占隐窝细胞总数的48.1±5.6%对30.1±8.5%;p<0.001)。还发现喂食乙醇后血清胃泌素浓度显著升高(172±51对106±27 pmol/l;p<0.01)。直肠黏膜中依赖乙醇的增殖变化预示着该部位对致癌作用的易感性更高,这支持了实验和流行病学数据。胃泌素浓度升高可能部分解释了观察到的直肠过度增殖。然而,其他可能的原因也不能排除。