Long-term iodine deficiency and excess inhibit β-casein and α-lactalbumin secretion of milk in lactating rats

IF 4.9 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Nutritional Biochemistry Pub Date : 2024-11-26 DOI:10.1016/j.jnutbio.2024.109812
Ying Zhang , Xin Zhao , Na Zhao , Yan Song , Zixuan Zhang , Xinbao Zhang , Haohao Meng , Xiru Wang , Le Shan , Wanqi Zhang , Zhongna Sang
{"title":"Long-term iodine deficiency and excess inhibit β-casein and α-lactalbumin secretion of milk in lactating rats","authors":"Ying Zhang ,&nbsp;Xin Zhao ,&nbsp;Na Zhao ,&nbsp;Yan Song ,&nbsp;Zixuan Zhang ,&nbsp;Xinbao Zhang ,&nbsp;Haohao Meng ,&nbsp;Xiru Wang ,&nbsp;Le Shan ,&nbsp;Wanqi Zhang ,&nbsp;Zhongna Sang","doi":"10.1016/j.jnutbio.2024.109812","DOIUrl":null,"url":null,"abstract":"<div><div>Iodine is critical for thyroid hormone synthesis and developmental programming in the first 1,000 days of life. The effect of maternal iodine on milk protein secretion remains unknown. We aimed to explore the effect of long-term maternal iodine deficiency and excess on milk protein secretion in lactating rats and its mechanisms preliminarily. Animal models of iodine deficiency and excess were generated by treating Wistar rats a low-iodine diet and deionized water with different potassium iodide concentrations from reproductive age to lactation. Under iodine deficiency, CSN2 and α-LA secretion of milk was inhibited in early and mid-lactation, respectively, and the inhibition of milk CSN2 and α-LA secretion weakened in late lactation. Under iodine excess, milk CSN2 secretion was inhibited in early lactation, and the inhibition of milk CSN2 and α-LA secretion was more pronounced in late lactation. Under iodine deficiency and excess, the concentrations of CSN2 and α-LA and protein expression levels of THRα1, THRβ1, and PRLR in the mammary gland decreased. These results demonstrate the negative impact of long-term maternal iodine malnutrition on milk protein secretion.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"137 ","pages":"Article 109812"},"PeriodicalIF":4.9000,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Nutritional Biochemistry","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0955286324002432","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Iodine is critical for thyroid hormone synthesis and developmental programming in the first 1,000 days of life. The effect of maternal iodine on milk protein secretion remains unknown. We aimed to explore the effect of long-term maternal iodine deficiency and excess on milk protein secretion in lactating rats and its mechanisms preliminarily. Animal models of iodine deficiency and excess were generated by treating Wistar rats a low-iodine diet and deionized water with different potassium iodide concentrations from reproductive age to lactation. Under iodine deficiency, CSN2 and α-LA secretion of milk was inhibited in early and mid-lactation, respectively, and the inhibition of milk CSN2 and α-LA secretion weakened in late lactation. Under iodine excess, milk CSN2 secretion was inhibited in early lactation, and the inhibition of milk CSN2 and α-LA secretion was more pronounced in late lactation. Under iodine deficiency and excess, the concentrations of CSN2 and α-LA and protein expression levels of THRα1, THRβ1, and PRLR in the mammary gland decreased. These results demonstrate the negative impact of long-term maternal iodine malnutrition on milk protein secretion.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
长期缺碘和碘过量都会抑制哺乳期大鼠乳汁中β-酪蛋白和α-乳白蛋白的分泌。
碘对甲状腺激素的合成和生命最初 1000 天的发育至关重要。母体碘对乳蛋白分泌的影响尚不清楚。我们旨在初步探讨母体长期碘缺乏和过量对哺乳期大鼠乳汁蛋白分泌的影响及其机制。通过给 Wistar 大鼠从育龄期到哺乳期喂食低碘食物和不同浓度碘化钾的去离子水,建立了碘缺乏和碘过量的动物模型。在碘缺乏的情况下,乳汁中CSN2和α-LA的分泌在泌乳早期和中期分别受到抑制,在泌乳晚期对乳汁中CSN2和α-LA分泌的抑制作用减弱。在碘过量的情况下,泌乳早期牛奶CSN2的分泌受到抑制,泌乳晚期对牛奶CSN2和α-LA分泌的抑制更明显。在碘缺乏和碘过量的情况下,乳腺中CSN2和α-LA的浓度以及THRα1、THRβ1和PRLR的蛋白表达水平均下降。这些结果表明了母体长期碘营养不良对乳汁蛋白质分泌的负面影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Journal of Nutritional Biochemistry
Journal of Nutritional Biochemistry 医学-生化与分子生物学
CiteScore
9.50
自引率
3.60%
发文量
237
审稿时长
68 days
期刊介绍: Devoted to advancements in nutritional sciences, The Journal of Nutritional Biochemistry presents experimental nutrition research as it relates to: biochemistry, molecular biology, toxicology, or physiology. Rigorous reviews by an international editorial board of distinguished scientists ensure publication of the most current and key research being conducted in nutrition at the cellular, animal and human level. In addition to its monthly features of critical reviews and research articles, The Journal of Nutritional Biochemistry also periodically publishes emerging issues, experimental methods, and other types of articles.
期刊最新文献
The interaction of ascorbic acid with hemoglobin: relevance to hemin release and lipid peroxidation. Fatty Acid Composition of Isoenergetic Meals Drives Distinct Postprandial Immunometabolic Responses in Healthy Adults: A Randomised Crossover Pilot Study. Dietary methylglyoxal induces renal lipotoxicity primarily through adipose tissue dysfunction in mice fed normal or obesogenic high-fat diets. Lnc-Gm26626 in visceral adipose tissues participates in energy metabolism via IDH3α-associated tricarboxylic acid cycle activity. Electroconvulsive therapy modulates brain plasticity in male depression: Links to gut microbial metabolites and diet-derived regulation of Wnt/BDNF signaling.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1