Department of Pediatrics, Selcuk University Faculty of Medicine, Konya, Turkey.
Department of Medical Biology, Medical Faculty, KTO Karatay University, Konya, Turkey.
Biol Trace Elem Res. 2024 May;202(5):2133-2142. doi: 10.1007/s12011-023-03824-8. Epub 2023 Sep 1.
The aim of this study was to investigate how zinc deficiency and supplementation affect liver markers including autotaxin, kallistatin, endocan, and zinc carrier proteins ZIP14 and ZnT9 in rats exposed to maternal zinc deficiency. Additionally, the study aimed to assess liver tissue damage through histological examination. A total of forty male pups were included in the research, with thirty originating from mothers who were given a zinc-deficient diet (Groups 1, 2, and 3), and the remaining ten born to mothers fed a standard diet (Group 4). Subsequently, Group 1 was subjected to a zinc-deficient diet, Group 2 received a standard diet, Group 3 received zinc supplementation, and Group 4 served as the control group without any supplementation. Upon completion of the experimental phases of the study, all animals were sacrificed under general anesthesia, and samples of liver tissue were obtained. The levels of autotaxin, kallistatin, endocan, ZIP 14, and ZnT9 in these liver tissue samples were determined using the ELISA technique. In addition, histological examination was performed to evaluate tissue damage in the liver samples. In the group experiencing zinc deficiency, both endocan and autotaxin levels increased compared to the control group. With zinc supplementation, the levels of endocan and autotaxin returned to the values observed in the control group. Similarly, the suppressed levels of kallistatin, ZIP14, and ZnT9 observed in the zinc deficiency group were reversed with zinc supplementation. Likewise, the reduced levels of kallistatin, ZIP14, and ZnT9 seen in the zinc deficiency group were rectified with zinc supplementation. Moreover, the application of zinc partially ameliorated the heightened liver tissue damage triggered by zinc deficiency. This study is the pioneering one to demonstrate that liver tissue dysfunction induced by a marginal zinc-deficient diet in rats with marginal maternal zinc deficiency can be alleviated through zinc supplementation.
本研究旨在探讨锌缺乏和补充对暴露于母体锌缺乏的大鼠肝脏标志物（包括自分泌酶、卡利斯塔丁、内钙蛋白和锌转运蛋白 ZIP14 和 ZnT9）的影响。此外，本研究还旨在通过组织学检查评估肝脏组织损伤。共有 40 只雄性幼鼠参与了这项研究，其中 30 只来自于接受缺锌饮食的母亲（第 1、2 和 3 组），其余 10 只来自于接受标准饮食的母亲（第 4 组）。随后，第 1 组接受缺锌饮食，第 2 组接受标准饮食，第 3 组接受锌补充，第 4 组作为无补充的对照组。研究的实验阶段完成后，所有动物在全身麻醉下被处死，并获取肝脏组织样本。使用 ELISA 技术测定这些肝组织样本中自分泌酶、卡利斯塔丁、内钙蛋白、ZIP14 和 ZnT9 的水平。此外，还进行了组织学检查以评估肝组织样本中的组织损伤。在缺锌组中，与对照组相比，内钙蛋白和自分泌酶的水平均升高。补锌后，内钙蛋白和自分泌酶的水平恢复到对照组观察到的水平。同样，缺锌组中观察到的 kallistatin、ZIP14 和 ZnT9 水平受抑制得到补锌纠正。同样，补锌纠正了缺锌组中 kallistatin、ZIP14 和 ZnT9 水平降低的情况。此外，锌的应用部分缓解了缺锌引起的肝脏组织损伤。本研究是首次证明，通过补锌可以缓解母体锌轻度缺乏的大鼠边缘性缺锌饮食引起的肝脏组织功能障碍。
