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与内质网应激、炎症和代谢紊乱相关的CCAAT/增强子结合蛋白β

CCAAT/enhancer binding protein β in relation to ER stress, inflammation, and metabolic disturbances.

作者信息

van der Krieken Sophie E, Popeijus Herman E, Mensink Ronald P, Plat Jogchum

机构信息

Department of Human Biology, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University, Universiteitssingel 50, P.O. Box 616, 6200 MD Maastricht, Netherlands.

出版信息

Biomed Res Int. 2015;2015:324815. doi: 10.1155/2015/324815. Epub 2015 Jan 28.

DOI:10.1155/2015/324815
PMID:25699273
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4324884/
Abstract

The prevalence of the metabolic syndrome and underlying metabolic disturbances increase rapidly in developed countries. Various molecular targets are currently under investigation to unravel the molecular mechanisms that cause these disturbances. This is done in attempt to counter or prevent the negative health consequences of the metabolic disturbances. Here, we reviewed the current knowledge on the role of C/EBP-β in these metabolic disturbances. C/EBP-β deletion in mice resulted in downregulation of hepatic lipogenic genes and increased expression of β-oxidation genes in brown adipose tissue. Furthermore, C/EBP-β is important in the differentiation and maturation of adipocytes and is increased during ER stress and proinflammatory conditions. So far, studies were only conducted in animals and in cell systems. The results found that C/EBP-β is an important transcription factor within the metabolic disturbances of the metabolic system. Therefore, it is interesting to examine the potential role of C/EBP-β at molecular and physiological level in humans.

摘要

在发达国家,代谢综合征及潜在的代谢紊乱的患病率迅速上升。目前正在研究各种分子靶点,以揭示导致这些紊乱的分子机制。这样做是为了对抗或预防代谢紊乱对健康造成的负面影响。在此,我们综述了目前关于C/EBP-β在这些代谢紊乱中作用的知识。小鼠体内C/EBP-β的缺失导致肝脏脂肪生成基因下调,棕色脂肪组织中β-氧化基因的表达增加。此外,C/EBP-β在脂肪细胞的分化和成熟中起重要作用,并且在内质网应激和促炎条件下会增加。到目前为止,研究仅在动物和细胞系统中进行。结果发现,C/EBP-β是代谢系统代谢紊乱中的一个重要转录因子。因此,研究C/EBP-β在人类分子和生理水平上的潜在作用很有意思。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d556/4324884/c0d85f06b2ff/BMRI2015-324815.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d556/4324884/a1acc46e53b9/BMRI2015-324815.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d556/4324884/0aa1b2b9411c/BMRI2015-324815.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d556/4324884/3f72fd5754fd/BMRI2015-324815.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d556/4324884/c0d85f06b2ff/BMRI2015-324815.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d556/4324884/a1acc46e53b9/BMRI2015-324815.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d556/4324884/0aa1b2b9411c/BMRI2015-324815.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d556/4324884/3f72fd5754fd/BMRI2015-324815.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d556/4324884/c0d85f06b2ff/BMRI2015-324815.004.jpg

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