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脂肪组织中 Ago2 介导的 microRNA 信号的差异表达与食物诱导的肥胖有关。

Differential expression of Ago2-mediated microRNA signaling in adipose tissue is associated with food-induced obesity.

机构信息

School of Life Science and Technology, Xinxiang Medical University, China.

Stem Cell and Biotherapy Technology Research Center, Xinxiang Medical University, China.

出版信息

FEBS Open Bio. 2022 Oct;12(10):1828-1838. doi: 10.1002/2211-5463.13471. Epub 2022 Sep 5.

DOI:10.1002/2211-5463.13471
PMID:36062491
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9527595/
Abstract

Adipose tissue is a major component for the regulation of energy homeostasis by storage and release of lipids. As a core element of RNA-induced silencing complex, argonaute2 (Ago2) plays critical role in maintenance of systemic metabolic demand. Here, we show that high-fat-diet-fed mice exhibit an increase in body mass alongside systematic insulin resistance and altered rate of energy expenditure. Interestingly, Ago2 expression is associated with obesity and an increased amount of adipose tissue. Moreover, increased levels of Ago2 inhibited the expression of AMPKα by promoting its targeting by miR-148a, the most abundant microRNA in adipose tissues. Those results suggested that Ago2-miR-148a-AMPKα signaling pathway play an important function in the developing obesity and adiposity, and will further provide basic research data for the potential clinical treatment of obesity.

摘要

脂肪组织是通过储存和释放脂质来调节能量平衡的主要成分。作为 RNA 诱导沉默复合物的核心元件,argonaute2(Ago2)在维持全身代谢需求方面发挥着关键作用。在这里,我们发现高脂肪饮食喂养的小鼠表现出体重增加,同时伴有系统性胰岛素抵抗和能量消耗率改变。有趣的是,Ago2 的表达与肥胖和脂肪组织量的增加有关。此外,Ago2 水平的升高通过促进其被脂肪组织中最丰富的 microRNA miR-148a 靶向,抑制了 AMPKα 的表达。这些结果表明,Ago2-miR-148a-AMPKα 信号通路在肥胖和肥胖症的发展中起着重要作用,并将为肥胖症的潜在临床治疗提供基础研究数据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b900/9527595/32e61b5acc24/FEB4-12-1828-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b900/9527595/096daa41496a/FEB4-12-1828-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b900/9527595/356caac242e7/FEB4-12-1828-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b900/9527595/a03e417a99d3/FEB4-12-1828-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b900/9527595/9cec330f91a7/FEB4-12-1828-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b900/9527595/32e61b5acc24/FEB4-12-1828-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b900/9527595/096daa41496a/FEB4-12-1828-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b900/9527595/356caac242e7/FEB4-12-1828-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b900/9527595/a03e417a99d3/FEB4-12-1828-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b900/9527595/9cec330f91a7/FEB4-12-1828-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b900/9527595/32e61b5acc24/FEB4-12-1828-g002.jpg

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本文引用的文献

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Adipocyte-secreted exosomal microRNA-34a inhibits M2 macrophage polarization to promote obesity-induced adipose inflammation.脂肪细胞分泌的细胞外体 microRNA-34a 抑制 M2 巨噬细胞极化,促进肥胖诱导的脂肪组织炎症。
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