The Adipocyte Acquires a Fibroblast-Like Transcriptional Signature in Response to a High Fat Diet
The Adipocyte Acquires a Fibroblast-Like Transcriptional Signature in Response to a High Fat Diet
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DOI：
10.1038/s41598-020-59284-w
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发表时间：
2020-02-11
影响因子：
4.6
通讯作者：
Farmer, Stephen R.
中科院分区：
文献类型：
--
作者：
Jones, Jessica E. C.;Rabhi, Nabil;Farmer, Stephen R.
内脏白色脂肪组织（vWAT）在饮食诱导的肥胖期间膨胀并经历广泛的重塑。关于各种基质血管细胞对重塑过程的贡献，我们知道得很多，但对脂肪细胞内发生的变化知之甚少，因为它变得逐渐功能失调。在这里，我们对分离的vWAT脂肪细胞进行了转录组分析，以评估慢性高脂饮食（HFD）引起的全局途径变化。数据表明，脂肪细胞通过采用成纤维细胞样表型响应HFD，其特征在于ECM、粘着斑和细胞骨架基因的表达增强以及许多脂肪细胞程序的抑制，最显著的是与线粒体相关的那些。这项研究表明，在肥胖症的脂肪细胞逐渐成为代谢功能障碍，由于其收购的纤维化功能。我们提出，机械响应转录因子，如MRTFA和SRF有助于上调形态基因以及抑制线粒体程序。
Visceral white adipose tissue (vWAT) expands and undergoes extensive remodeling during diet-induced obesity. Much is known about the contribution of various stromal vascular cells to the remodeling process, but less is known of the changes that occur within the adipocyte as it becomes progressively dysfunctional. Here, we performed a transcriptome analysis of isolated vWAT adipocytes to assess global pathway changes occurring in response to a chronic high fat diet (HFD). The data demonstrate that the adipocyte responds to the HFD by adopting a fibroblast-like phenotype, characterized by enhanced expression of ECM, focal adhesion and cytoskeletal genes and suppression of many adipocyte programs most notably those associated with mitochondria. This study reveals that during obesity the adipocyte progressively becomes metabolically dysfunctional due to its acquisition of fibrogenic functions. We propose that mechano-responsive transcription factors such as MRTFA and SRF contribute to both upregulation of morphological genes as well as suppression of mitochondrial programs.