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小鼠哺乳期组织锌库的重新分布及边缘性锌缺乏时的体内稳态失调

Redistribution of tissue zinc pools during lactation and dyshomeostasis during marginal zinc deficiency in mice.

作者信息

McCormick Nicholas H, King Janet, Krebs Nancy, Soybel David I, Kelleher Shannon L

机构信息

Department of Nutritional Sciences, The Pennsylvania State University, University Park, PA 16802, USA.

Children's Hospital Oakland Research Institute, Oakland, CA 94609, USA.

出版信息

J Trace Elem Med Biol. 2015 Jan;29:170-5. doi: 10.1016/j.jtemb.2014.06.002. Epub 2014 Jun 11.

DOI:10.1016/j.jtemb.2014.06.002
PMID:24974135
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4258524/
Abstract

Zinc (Zn) requirements are increased during lactation. Increased demand is partially met through increased Zn absorption from the diet. It is estimated that 60-80% of women of reproductive age are at risk for Zn deficiency due to low intake of bioavailable Zn and increased demands during pregnancy and lactation. How Zn is redistributed within the body to meet the demands of lactation, and how Zn deficiency affects this process, is not understood. Female C57bl/6J mice were fed a control (ZA; 30mg Zn/kg) or a marginally Zn deficient (ZD; 15mg Zn/kg) diet for 30 days prior to mating through mid-lactation and compared with nulliparous mice fed the same diets. While stomach and plasma Zn concentration increased during lactation in mice fed ZA, mice fed ZD had lower stomach Zn concentration and abrogated plasma Zn levels during lactation. Additionally, femur Zn decreased during lactation in mice fed ZA, while mice fed ZD did not experience this decrease. Furthermore, red blood cell, pancreas, muscle and mammary gland Zn concentration increased, and liver and adrenal gland Zn decreased during lactation, independent of diet, while kidney Zn concentration increased only in mice fed ZD. Finally, maternal Zn deficiency significantly increased the liver Zn concentration in offspring but decreased weight gain and survival. This study provides novel insight into how Zn is redistributed to meet the increased metabolic demands of lactation and how marginal Zn deficiency interferes with these homeostatic adjustments.

摘要

哺乳期对锌(Zn)的需求量会增加。通过增加从饮食中吸收锌,可部分满足这种增加的需求。据估计,60 - 80%的育龄女性因生物可利用锌摄入量低以及孕期和哺乳期需求增加而面临锌缺乏风险。锌在体内如何重新分配以满足哺乳期的需求,以及锌缺乏如何影响这一过程,目前尚不清楚。在交配前至哺乳期中期,给雌性C57bl/6J小鼠喂食对照饮食(ZA;30毫克锌/千克)或轻度缺锌饮食(ZD;15毫克锌/千克)30天,并与喂食相同饮食的未生育小鼠进行比较。虽然喂食ZA的小鼠在哺乳期胃和血浆锌浓度增加,但喂食ZD的小鼠在哺乳期胃锌浓度较低且血浆锌水平消失。此外,喂食ZA的小鼠在哺乳期股骨锌含量下降,而喂食ZD的小鼠未出现这种下降。此外,红细胞、胰腺、肌肉和乳腺的锌浓度在哺乳期增加,肝脏和肾上腺的锌浓度下降,且与饮食无关,而肾脏锌浓度仅在喂食ZD的小鼠中增加。最后,母体锌缺乏显著增加了后代肝脏锌浓度,但降低了体重增加和存活率。这项研究为锌如何重新分配以满足哺乳期增加的代谢需求以及轻度锌缺乏如何干扰这些体内平衡调节提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/4258524/602709805d9c/nihms608996f7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/4258524/602709805d9c/nihms608996f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1a0d/4258524/0a606c88ffc4/nihms608996f1.jpg
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Dietary zinc deficiency exaggerates ethanol-induced liver injury in mice: involvement of intrahepatic and extrahepatic factors.膳食锌缺乏可加重乙醇诱导的小鼠肝损伤:涉及肝内和肝外因素。
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Gastric and colonic zinc transporter ZIP11 (Slc39a11) in mice responds to dietary zinc and exhibits nuclear localization.
边缘性膳食锌缺乏会加剧脓毒症诱导的骨骼肌肿瘤坏死因子-α的改变,但不会影响蛋白质合成。
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