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肝脂肪变性时锌和铜的代谢异常。

Abnormal zinc and copper metabolism in hepatic steatosis.

作者信息

Mikhail T H, Nicola W G, Ibrahim K H, Salama S H, Emam M

机构信息

Physiology unit, National Research Centre.

出版信息

Boll Chim Farm. 1996 Nov;135(10):591-7.

PMID:9048448
Abstract

Abnormal Zinc and Copper metabolism were studied in rats with tetracycline-induced fatty liver and compared with normal rats. The present work recorded decreased serum zinc concentration with increased copper concentration in the tetracycline-injected rats. The results also showed that the liver and heart zinc were significantly decreased; meanwhile it was observed that the concentration of zinc in the kidney tissue of fatty liver rats was significantly raised in comparison with those of normal rats. Histopathological studies of the kidney tissue showed degenerative changes in the tables with areas of focal necrosis. Renal tubular necrosis in such cases is largely caused by the toxic degradation products of tetracycline metabolism. The kidney lesion together with impaired gastrointestinal absorption contributed to the hypozincaemia observed in the present results. Although the present data showed a significant reduction in serum zinc and significant rise in plasma insulin in the fatty liver rats there was nonsignificant correlation between the two variables as compared with the normal rats. The positive correlation between serum zinc concentration and reduced high-density lipoprotein cholesterol (HDL-C) emphasizes the role of zinc deficiency in atherosclerotic disease in fatty liver.

摘要

研究了四环素诱导的脂肪肝大鼠的锌和铜代谢异常,并与正常大鼠进行了比较。目前的研究记录了注射四环素的大鼠血清锌浓度降低,铜浓度升高。结果还表明,肝脏和心脏中的锌显著降低;同时观察到,与正常大鼠相比,脂肪肝大鼠肾脏组织中的锌浓度显著升高。肾脏组织的组织病理学研究显示,肾小管出现退行性变化,并伴有局灶性坏死区域。在这种情况下,肾小管坏死主要是由四环素代谢的有毒降解产物引起的。肾脏病变以及胃肠道吸收受损导致了本研究结果中观察到的低锌血症。尽管目前的数据显示脂肪肝大鼠血清锌显著降低,血浆胰岛素显著升高,但与正常大鼠相比,这两个变量之间没有显著相关性。血清锌浓度与高密度脂蛋白胆固醇(HDL-C)降低之间的正相关强调了锌缺乏在脂肪肝动脉粥样硬化疾病中的作用。

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