Goodlad R A, Al-Mukhtar M Y, Ghatei M A, Bloom S R, Wright N A
Virchows Arch B Cell Pathol Incl Mol Pathol. 1983;43(1):55-62. doi: 10.1007/BF02932943.
The effects of starvation and refeeding on intestinal cell proliferation at several sites of the rat gastrointestinal tract were studied and used as a model of altered cell proliferation in order to investigate the relationship between the rate of cell production and plasma gastrin and enteroglucagon. There was a marked fall in crypt cell production rate after four days starvation, with the proximal sites of the gut being most affected. The response to refeeding varied with site, suggesting that there was more than one mechanism for the control of intestinal cell proliferation. Plasma gastrin and enteroglucagon both fell to one fifth of their control level after starvation. Plasma gastrin increased slowly after refeeding, whilst plasma enteroglucagon increased rapidly to values significantly above control. Plasma gastrin was only correlated with crypt cell production in the duodenum, while plasma enteroglucagon was correlated with crypt cell production rate at several sites, indicating that enteroglucagon may be involved in the control of intestinal cell production.
研究了饥饿和再喂养对大鼠胃肠道多个部位肠细胞增殖的影响,并将其作为细胞增殖改变的模型,以研究细胞产生速率与血浆胃泌素和肠高血糖素之间的关系。饥饿四天后隐窝细胞产生速率显著下降,肠道近端部位受影响最大。再喂养后的反应因部位而异,这表明控制肠细胞增殖的机制不止一种。饥饿后血浆胃泌素和肠高血糖素均降至对照水平的五分之一。再喂养后血浆胃泌素缓慢增加,而血浆肠高血糖素迅速增加至显著高于对照的值。血浆胃泌素仅与十二指肠隐窝细胞产生相关,而血浆肠高血糖素与多个部位的隐窝细胞产生速率相关,表明肠高血糖素可能参与肠细胞产生的控制。