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白色脂肪组织对维生素B3缺乏的转录反应

Transcriptional Response of White Adipose Tissue to Withdrawal of Vitamin B3.

作者信息

Shi Wenbiao, Hegeman Maria A, Doncheva Atanaska, van der Stelt Inge, Bekkenkamp-Grovenstein Melissa, van Schothorst Evert M, Brenner Charles, de Boer Vincent C J, Keijer Jaap

机构信息

Human and Animal Physiology, Wageningen University, PO Box 338, 6700, AH, Wageningen, The Netherlands.

Educational Consultancy & Professional Development, Faculty of Social and Behavioural Sciences, Utrecht University, 3584, CS, Utrecht, The Netherlands.

出版信息

Mol Nutr Food Res. 2019 Jul;63(13):e1801100. doi: 10.1002/mnfr.201801100. Epub 2019 Apr 26.

DOI:10.1002/mnfr.201801100
PMID:30990964
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6618275/
Abstract

SCOPE

Distinct markers for mild vitamin B3 deficiency are lacking. To identify these, the molecular responses of white adipose tissue (WAT) to vitamin B3 withdrawal are examined.

METHODS AND RESULTS

A dietary intervention is performed in male C57BL/6JRccHsd mice, in which a diet without nicotinamide riboside (NR) is compared to a diet with NR at the recommended vitamin B3 level. Both diets contain low but adequate level of tryptophan. Metabolic flexibility and systemic glucose tolerance are analyzed and global transcriptomics, qRT-PCR, and histology of epididymal WAT (eWAT) are performed. A decreased insulin sensitivity and a shift from carbohydrate to fatty acid oxidation in response to vitamin B3 withdrawal are observed. This is consistent with molecular changes in eWAT, including an activated MEK/ERK signaling, a lowering of glucose utilization markers, and an increase in makers of fatty acid catabolism, possibly related to the consistent lower expression of mitochondrial electron transport complexes. The synthesis pathway of tetrahydropteridine (BH4), an essential cofactor for neurotransmitter synthesis, is transcriptionally activated. Genes marking these processes are technically validated.

CONCLUSION

The downregulation of Anp32a, Tnk2 and the upregulation of Mapk1, Map2k1, Qdpr, Mthfs, and Mthfsl are proposed as a WAT transcriptional signature marker for mild vitamin B3 deficiency.

摘要

范围

目前缺乏轻度维生素B3缺乏的特异性标志物。为了识别这些标志物，研究了白色脂肪组织（WAT）对维生素B3缺乏的分子反应。

方法与结果

对雄性C57BL/6JRccHsd小鼠进行饮食干预，将不含烟酰胺核糖（NR）的饮食与含有推荐维生素B3水平的NR饮食进行比较。两种饮食都含有低但充足水平的色氨酸。分析代谢灵活性和全身葡萄糖耐量，并对附睾白色脂肪组织（eWAT）进行全转录组学、qRT-PCR和组织学分析。观察到维生素B3缺乏导致胰岛素敏感性降低以及从碳水化合物氧化向脂肪酸氧化的转变。这与eWAT中的分子变化一致，包括MEK/ERK信号激活、葡萄糖利用标志物降低以及脂肪酸分解标志物增加，这可能与线粒体电子传递复合体的持续低表达有关。神经递质合成必需辅因子四氢生物蝶呤（BH4）的合成途径被转录激活。标记这些过程的基因在技术上得到了验证。

结论

Anp32a、Tnk2的下调以及Mapk1、Map2k1、Qdpr、Mthfs和Mthfsl的上调被提议作为轻度维生素B3缺乏的WAT转录特征标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/735d/6618275/a8fa4610ae9f/MNFR-63-na-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/735d/6618275/329a222f4535/MNFR-63-na-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/735d/6618275/899b5127e97a/MNFR-63-na-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/735d/6618275/547cafc7a010/MNFR-63-na-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/735d/6618275/a8fa4610ae9f/MNFR-63-na-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/735d/6618275/329a222f4535/MNFR-63-na-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/735d/6618275/8e5e106aca96/MNFR-63-na-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/735d/6618275/43a08249f7e7/MNFR-63-na-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/735d/6618275/547cafc7a010/MNFR-63-na-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/735d/6618275/a8fa4610ae9f/MNFR-63-na-g008.jpg

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