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2
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本文引用的文献

1
Regulation of Adipogenesis and Key Adipogenic Gene Expression by 1, 25-Dihydroxyvitamin D in 3T3-L1 Cells.1,25-二羟基维生素D对3T3-L1细胞脂肪生成及关键脂肪生成基因表达的调控
PLoS One. 2015 Jun 1;10(6):e0126142. doi: 10.1371/journal.pone.0126142. eCollection 2015.
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Impact of maternal obesity on fetal programming of cardiovascular disease.母亲肥胖对心血管疾病胎儿编程的影响。
Physiology (Bethesda). 2015 May;30(3):224-31. doi: 10.1152/physiol.00021.2014.
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Considering maternal dietary modulators for epigenetic regulation and programming of the fetal epigenome.考虑母体饮食调节剂对胎儿表观基因组的表观遗传调控和编程。
Nutrients. 2015 Apr 14;7(4):2748-70. doi: 10.3390/nu7042748.
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Expression patterns of transcription factor PPARγ and C/EBP family members during in vitro adipogenesis of human bone marrow mesenchymal stem cells.人骨髓间充质干细胞体外脂肪生成过程中转录因子PPARγ和C/EBP家族成员的表达模式
Cell Biol Int. 2015 Apr;39(4):457-65. doi: 10.1002/cbin.10415. Epub 2015 Feb 2.
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Beyond regulatory T cells: the potential role for IL-2 to deplete T-follicular helper cells and treat autoimmune diseases.超越调节性T细胞:白细胞介素-2在耗竭滤泡辅助性T细胞及治疗自身免疫性疾病中的潜在作用
Immunotherapy. 2014;6(11):1207-20. doi: 10.2217/imt.14.83.
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Transcriptional regulation of adipocyte differentiation: a central role for CCAAT/enhancer-binding protein (C/EBP) β.脂肪细胞分化的转录调控:CCAAT/增强子结合蛋白(C/EBP)β的核心作用。
J Biol Chem. 2015 Jan 9;290(2):755-61. doi: 10.1074/jbc.R114.619957. Epub 2014 Dec 1.
7
Maternal vitamin D deficiency and fetal programming--lessons learned from humans and mice.母体维生素D缺乏与胎儿编程——从人类和小鼠身上获得的经验教训
Kidney Blood Press Res. 2014;39(4):315-29. doi: 10.1159/000355809. Epub 2014 Sep 19.
8
Developmental programming and transgenerational transmission of obesity.肥胖的发育编程与跨代传递
Ann Nutr Metab. 2014;64 Suppl 1:26-34. doi: 10.1159/000360506. Epub 2014 Jul 23.
9
PPARγ and the global map of adipogenesis and beyond.过氧化物酶体增殖物激活受体 γ 与脂肪生成的全局图谱及其拓展。
Trends Endocrinol Metab. 2014 Jun;25(6):293-302. doi: 10.1016/j.tem.2014.04.001. Epub 2014 Apr 29.
10
Obesity and its metabolic complications: the role of adipokines and the relationship between obesity, inflammation, insulin resistance, dyslipidemia and nonalcoholic fatty liver disease.肥胖及其代谢并发症:脂肪因子的作用以及肥胖、炎症、胰岛素抵抗、血脂异常与非酒精性脂肪性肝病之间的关系。
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孕期母体维生素 D 缺乏影响瘦素雄性小鼠后代脂肪生成调节基因过氧化物酶体增殖物激活受体γ(PPARγ)和维生素 D 受体(VDR)的表达。

Maternal vitamin D deficiency during pregnancy affects expression of adipogenic-regulating genes peroxisome proliferator-activated receptor gamma (PPARγ) and vitamin D receptor (VDR) in lean male mice offspring.

机构信息

Department of Nutrition and Exercise Physiology, University of Missouri, 204 Gwynn Hall, Columbia, MO, 65211, USA.

MIND Institute, University of California, Davis, 2825 50th St, Sacramento, CA, 95817, USA.

出版信息

Eur J Nutr. 2018 Mar;57(2):723-730. doi: 10.1007/s00394-016-1359-x. Epub 2016 Dec 21.

DOI:10.1007/s00394-016-1359-x
PMID:28004271
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6643277/
Abstract

PURPOSE

Maternal vitamin D deficiency during pregnancy is a widespread issue that may have long-lasting consequences on offspring adiposity. We sought to determine how maternal vitamin D deficiency during the perinatal period would affect offspring adipose tissue development and gene expression.

METHODS

Female C57BL/6 J mice were fed either a vitamin D deficient (VDD) or control diet from 4 weeks before pregnancy (periconception) until 7 days postparturition. Male offspring were weighed and euthanized at 75 days of age (early adult period), at which point serum was collected for biochemical analyses, and perigonadal and subcutaneous white adipose tissue (PGAT and SQAT, respectively) were excised, weighed, then flash-frozen for later histology and analyses of adipogenic gene expression.

RESULTS

All adult male offspring were nonobese; there were no significant differences in body weight, adipose pad weight, or adipocyte size. However, VDD-exposed offspring had greater expression of the adipogenic-regulating genes peroxisome proliferator-activated receptor gamma (Pparg) and vitamin D receptor (Vdr).

CONCLUSIONS

This study suggests that exposure to vitamin D deficiency during the perinatal period can directly affect genes involved in the development of adipose tissue in nonobese offspring. These novel findings invite further investigation into the mechanisms by which maternal vitamin D status during pregnancy affects adipose development and metabolic health of offspring.

摘要

目的

孕期母体维生素 D 缺乏是一个普遍存在的问题,可能对后代的肥胖产生持久影响。我们试图确定围产期母体维生素 D 缺乏如何影响后代脂肪组织发育和基因表达。

方法

从受孕前 4 周(围孕期)到产后 7 天,雌性 C57BL/6J 小鼠分别喂食维生素 D 缺乏(VDD)或对照饮食。雄性后代在 75 天大(成年早期)时称重并安乐死,此时收集血清进行生化分析,并切除性腺周和皮下白色脂肪组织(PGAT 和 SQAT),称重,然后立即冷冻用于组织学和脂肪生成基因表达分析。

结果

所有成年雄性后代均非肥胖;体重、脂肪垫重量或脂肪细胞大小无显著差异。然而,VDD 暴露的后代具有更高的脂肪生成调节基因过氧化物酶体增殖物激活受体 γ(Pparg)和维生素 D 受体(Vdr)的表达。

结论

本研究表明,围产期暴露于维生素 D 缺乏可直接影响非肥胖后代脂肪组织发育相关基因。这些新发现促使进一步研究孕期母体维生素 D 状态如何影响后代脂肪发育和代谢健康的机制。