Yeh K Y, Yeh M, Holt P R
Division of Gastroenterology, St. Luke's-Roosevelt Hospital Center, New York, New York 10025.
Am J Physiol. 1987 Dec;253(6 Pt 1):G802-8. doi: 10.1152/ajpgi.1987.253.6.G802.
Adaptive growth and precocious expression of sucrase activity occur in the small intestine of artificially reared (AR) rat pups fed a hormone-free diet. The physiological mechanisms underlying adaptive intestinal growth were studied. Day 12 rat pups that received jejunal isografts subcutaneously on day 0 were subjected to artificial feeding and were killed on day 16. Crypt cellularity and DNA labeling index in isografts from AR, but not from mother-fed, rats increased significantly to levels found in in situ host jejunum of AR rats, indicating that humoral regulatory mechanisms are responsible for intestinal cell proliferation in AR pups. Radioimmunoassays of serum corticosterone, thyroxine, insulin, and gastrin and of gastric gastrin contents revealed that only serum corticosterone concentrations were significantly elevated, suggesting that corticosterone plays a critical role for intestinal growth. To examine this possibility directly, day 12 rats were adrenalectomized (ADX) and AR by continuous infusion of diets containing 0, 10, or 50 micrograms/ml corticosterone. Serum corticosterone concentrations paralleled the infused doses of corticosterone. Jejunal DNA labeling index increased in all ADX AR rats at day 13 in a dose-dependent manner. Increased jejunal DNA labeling index was maintained on day 14 in intact AR rats and ADX AR rats fed 10 micrograms/ml corticosterone but not in ADX AR rats receiving 0 or 50 micrograms/ml. We conclude that endogenous corticosterone is one of the systemic factors responsible for the adaptive increase in intestinal growth of AR rats.
在喂食无激素饮食的人工饲养(AR)大鼠幼崽的小肠中,会出现适应性生长和蔗糖酶活性的早熟表达。对适应性肠道生长的生理机制进行了研究。在第0天接受空肠同基因移植皮下植入的第12天大鼠幼崽,进行人工饲养,并于第16天处死。AR大鼠而非由母鼠喂养的大鼠的同基因移植组织中的隐窝细胞密度和DNA标记指数显著增加,达到AR大鼠原位宿主空肠中的水平,这表明体液调节机制负责AR幼崽的肠道细胞增殖。对血清皮质酮、甲状腺素、胰岛素和胃泌素以及胃内胃泌素含量的放射免疫分析显示,只有血清皮质酮浓度显著升高,这表明皮质酮对肠道生长起关键作用。为了直接检验这种可能性,对第12天的大鼠进行肾上腺切除术(ADX),并通过持续输注含0、10或50微克/毫升皮质酮的饮食进行人工饲养。血清皮质酮浓度与输注的皮质酮剂量平行。在第13天,所有ADX AR大鼠的空肠DNA标记指数均呈剂量依赖性增加。在第14天,完整的AR大鼠和喂食10微克/毫升皮质酮的ADX AR大鼠的空肠DNA标记指数保持升高,但接受0或50微克/毫升皮质酮的ADX AR大鼠则不然。我们得出结论,内源性皮质酮是导致AR大鼠肠道生长适应性增加的全身因素之一。