Wu J Y, Reaves S K, Wang Y R, Wu Y, Lei P P, Lei K Y
Department of Nutritional Sciences, University of Arizona, Tucson, Arizona 85721, USA.
Am J Physiol. 1998 Dec;275(6):C1516-25. doi: 10.1152/ajpcell.1998.275.6.C1516.
The influence of Zn deficiency on the plasma level as well as the hepatic and intestinal gene expression of apolipoprotein (apo) A-I was examined in rats and hamsters. Male Sprague-Dawley rats (8 wk old) and Golden Syrian hamsters (7 wk old) were assigned to three dietary treatments: Zn adequate (ZA, 30 mg Zn/kg diet), Zn deficient (ZD, <0.5 mg Zn/kg diet), and Zn replete (ZDA, ZD animals fed the ZA diet for the last 2 days). The dietary treatments lasted for 18 days for rats or 6 wk for hamsters. For the measurement of apoA-I mRNA abundance, hamster apoA-I cDNA was cloned from the small intestine. The full-length 905-base pair cDNA shared approximately 80% similarity with the human, rat, and mouse apoA-I cDNAs. Hepatic and plasma Zn levels were reduced in ZD animals but normalized in ZDA rats and increased in ZDA hamsters compared with ZA animals. Zn deficiency reduced plasma apoA-I and hepatic apoA-I mRNA levels 13 and 38%, respectively, in ZD rats. The 2 days of Zn replenishment raised plasma apoA-I and hepatic apoA-I mRNA levels in ZDA rats by 34 and 28%, respectively, higher than ZA rats. Similarly, these levels were decreased by 18 and 25%, respectively, in ZD hamsters but normalized in ZDA hamsters compared with ZA hamsters. In contrast to the alterations of hepatic apoA-I mRNA levels, neither Zn deficiency nor subsequent Zn repletion produced alterations in the intestinal apoA-I mRNA abundance. Data from this study demonstrated that Zn deficiency specifically decreases hepatic apoA-I gene expression, which may at least be partly responsible for the reduction of plasma apoA-I levels.
在大鼠和仓鼠中研究了锌缺乏对血浆水平以及载脂蛋白（apo）A-I的肝脏和肠道基因表达的影响。将雄性斯普拉格-道利大鼠（8周龄）和金黄叙利亚仓鼠（7周龄）分为三种饮食处理组：锌充足（ZA，30毫克锌/千克饮食）、锌缺乏（ZD，< 0.5毫克锌/千克饮食）和锌补充（ZDA，ZD动物在最后2天喂食ZA饮食）。饮食处理对大鼠持续18天，对仓鼠持续6周。为了测量apoA-I mRNA丰度，从小肠克隆了仓鼠apoA-I cDNA。全长905个碱基对的cDNA与人类、大鼠和小鼠的apoA-I cDNA具有约80%的相似性。与ZA动物相比，ZD动物的肝脏和血浆锌水平降低，但ZDA大鼠的锌水平恢复正常，ZDA仓鼠的锌水平升高。锌缺乏使ZD大鼠的血浆apoA-I和肝脏apoA-I mRNA水平分别降低了13%和38%。锌补充2天使ZDA大鼠的血浆apoA-I和肝脏apoA-I mRNA水平分别比ZA大鼠提高了34%和28%。同样，与ZA仓鼠相比，ZD仓鼠的这些水平分别降低了18%和25%，但ZDA仓鼠的水平恢复正常。与肝脏apoA-I mRNA水平的变化相反，锌缺乏和随后的锌补充均未引起肠道apoA-I mRNA丰度的改变。本研究数据表明，锌缺乏特异性降低肝脏apoA-I基因表达，这可能至少部分导致血浆apoA-I水平降低。
