Depletion of liver and esophageal epithelium vitamin a after chronic moderate ethanol consumption in rats: Inverse relation to zinc nutriture
Depletion of liver and esophageal epithelium vitamin a after chronic moderate ethanol consumption in rats: Inverse relation to zinc nutriture
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大鼠慢性适度乙醇消耗后肝脏和食管上皮维生素 A 的消耗：与锌营养成反比
作者：
S. Mobarhan;T. Layden;H. Friedman;A. Kunigk;Philip Donahue
本研究旨在确定慢性中度酒精摄入是否会改变肝脏和食管上皮的维生素A水平，以及这是否依赖于锌营养状况。将40只4周龄雄性Sprague-道利大鼠分为5组：缺锌（0.9 ppm），乙醇喂养;缺锌;锌充足（25 ppm）;锌充足（25 ppm），乙醇喂养;和锌补充（50 ppm），乙醇喂养。所有大鼠均接受含有4，000 IU/L维生素A的Lieber-DeCarli液体饲料，持续5周。缺锌、乙醇喂养大鼠和锌充足、乙醇喂养大鼠和锌补充、乙醇喂养大鼠接受15.5%的热量摄入作为乙醇，而缺锌和锌充足大鼠接受等热量的麦芽糖糊精。所有组均配对喂养缺锌、乙醇喂养的大鼠。此外，对指定为体重限制对照组的一组8只大鼠喂食与锌充足大鼠相似的饲料，但其量与缺锌组相同，以获得最终体重。35天后，所有大鼠的肝脏组织学均正常，未观察到脂肪蓄积。与对照组（137 ± 49）相比，锌充足的乙醇喂养大鼠（41 ± 10 μg/gm）和补充锌的乙醇喂养大鼠（12 ± 5 μg/gm）的肝脏维生素A浓度显著降低。在乙醇喂养的动物中发现血清锌和肝脏维生素A之间存在高度显著的负相关性。在缺锌、乙醇喂养的大鼠中，乙醇没有诱导肝脏维生素A的动员，但是，与对照组相比，它导致视黄酯与视黄醇的比值显著降低（53 ± 16%）。在不饮酒的情况下缺锌导致肝脏维生素A浓度和总含量降低，这种影响不是继发于蛋白质热量营养不良，因为体重限制对照组的值不受影响。在食道上皮中，与对照组（3.3 ± 1.0，p < 0.01）相比，补充锌、饲喂乙醇的大鼠中维生素A储存显着减少（0.67 ± 0.7 μg/gm），并且观察到血清锌与食道维生素A之间显着负相关性饲喂乙醇的大鼠的维生素A水平。这些结果表明，适量的乙醇会导致肝脏和食管维生素A状态的深刻改变，这些影响与锌营养状况呈负相关。
This study was designed to determine whether chronic moderate ethanol ingestion alters the levels of vitamin A of liver and esophageal epithelium and if this is dependent on zinc nutriture. Forty male Sprague‐Dawley 4‐week‐old rats were divided into five groups: zinc‐deficient (0.9 ppm), ethanol‐fed; zinc‐deficient; zinc‐adequate (25 ppm); zinc‐adequate (25 ppm), ethanol‐fed; and zinc‐supplemented (50 ppm), ethanol‐fed. All rats received liquid Lieber‐DeCarli diet containing 4,000 IU per liter of vitamin A for 5 weeks. Zinc‐deficient, ethanol‐fed rats and zinc‐adequate, ethanol‐fed rats and zinc‐supplemented, ethanol‐fed rats received 15.5% of the caloric intake as ethanol while zinc‐deficient and zinc‐adequate rats received isocaloric amounts of maltose dextrin. All groups were pair‐fed to zinc‐deficient, ethanol‐fed rats. In addition, a group of eight rats designated as weight‐restricted controls were fed a diet similar to the one given to zinc‐adequate rats but in the amount to obtain a final weight as in the zinc‐deficient group. After 35 days, the liver histology was normal in all rats, and no fat accumulation was noted. Hepatic vitamin A concentration was significantly decreased in zinc‐adequate, ethanol‐fed rats (41 ± 10 μg per gm) and further in zinc‐supplemented, ethanol‐fed rats (12 ± 5 μg per gm) as compared to controls (137 ± 49). A highly significant negative correlation between serum zinc and liver vitamin A was found in ethanol‐fed animals. In zinc‐deficient, ethanol‐fed rats, ethanol did not induce mobilization of liver vitamin A, however, it caused a significant reduction in the ratio of retinyl ester to retinol (53 ± 16%) as compared to controls. Zinc deficiency in the absence of alcohol caused a reduction of hepatic vitamin A concentration and total content, and this effect was not secondary to protein‐caloric malnutrition as values were unaffected in weight‐restricted controls. In esophageal epithelium, a significant reduction of vitamin A stores was noted in zinc‐supplemented, ethanol‐fed rats (0.67 ± 0.7 μg per gm) as compared to controls (3.3 ± 1.0, p < 0.01), and a significant negative correlation was seen between serum zinc and esophageal vitamin A levels of ethanol‐fed rats. These results demonstrate that ethanol in moderate quantities causes profound alterations of the vitamin A status of the liver and esophagus, and these effects are inversely correlated to zinc nutriture.
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