Nobili F, Vignolini F, Figus E, Mengheri E
Istituto Nazionale della Nutrizione, 00178 Rome, Italy.
J Nutr. 1997 Sep;127(9):1807-13. doi: 10.1093/jn/127.9.1807.
Structural and functional damage to the intestine and the potential beneficial effects of dexamethasone (Dex) and thyroxine (T4) were examined in zinc-deficient rats. Rats were assigned to zinc deficient (ZD), control (C) or pair-fed (PF ) groups and fed for 40 d a zinc deficient (1 mg/kg) diet (ZD rats) or a similar diet supplemented with 50 mg Zn/kg (C and PF rats). Some rats of the ZD group were treated for the last 10 d with low (250 mg/kg) or high (5 mg/kg) doses of Dex or with T4 (100 mg/kg). Serum corticosterone of T4-treated ZD rats did not differ from untreated ZD rats. Serum T4 of T4-treated ZD rats did not differ from C rats. ZD rats developed ulcerations, inflammation and edema in the small intestine, particularly in the jejunum. PF rats did not show mucosal changes relative to C rats. ZD rats showed significantly lower crypt cell production rate (CCPR) and labeling index (LI) in the three intestinal regions, and lower cell migration rate and higher turnover time in the duodenum relative to C rats. Sucrase and maltase activities of ZD rats were significantly lower than C rats in the three mucosal regions. Treatment with the low dose of Dex resulted in fewer ulcerations compared with ZD rats. In rats administered the high dose of Dex or T4, all morphological alterations disappeared; the CCPR, LI, cell migration rate, cell turnover time and disaccharidase activities did not differ from C rats. In conclusion, Dex and T4 exert beneficial effects on zinc deficiency-induced intestinal alterations in rats.
在缺锌大鼠中研究了肠道的结构和功能损伤以及地塞米松（Dex）和甲状腺素（T4）的潜在有益作用。将大鼠分为缺锌（ZD）、对照（C）或配对喂养（PF）组，用缺锌（1mg/kg）饮食喂养40天（ZD大鼠）或用补充50mg Zn/kg的类似饮食喂养（C和PF大鼠）。ZD组的一些大鼠在最后10天用低剂量（250mg/kg）或高剂量（5mg/kg）的Dex或T4（100mg/kg）进行治疗。T4治疗的ZD大鼠血清皮质酮与未治疗的ZD大鼠无差异。T4治疗的ZD大鼠血清T4与C大鼠无差异。ZD大鼠在小肠，特别是空肠出现溃疡、炎症和水肿。PF大鼠相对于C大鼠未显示黏膜变化。相对于C大鼠，ZD大鼠在三个肠道区域的隐窝细胞产生率（CCPR）和标记指数（LI）显著降低，十二指肠的细胞迁移率较低，周转时间较长。ZD大鼠在三个黏膜区域的蔗糖酶和麦芽糖酶活性显著低于C大鼠。与ZD大鼠相比，低剂量Dex治疗导致的溃疡较少。在给予高剂量Dex或T4的大鼠中，所有形态学改变均消失；CCPR、LI、细胞迁移率、细胞周转时间和双糖酶活性与C大鼠无差异。总之，Dex和T4对缺锌诱导的大鼠肠道改变具有有益作用。
