File Download

There are no files associated with this item.

  • Find it @ UNIST can give you direct access to the published full text of this article. (UNISTARs only)
Related Researcher

박지영

Park, Jiyoung
Molecular Metabolism Lab.
Read More

Views & Downloads

Detailed Information

Cited time in webofscience Cited time in scopus
Metadata Downloads

Endotrophin triggers adipose tissue fibrosis and metabolic dysfunction

Author(s)
Sun, KaiPark, JiyoungGupta, Olga T.Holland, William L.Auerbach, PernilleZhang, NingyanMarangoni, Roberta GoncalvesNicoloro, Sarah M.Czech, Michael P.Varga, JohnPloug, ThorkilAn, ZhiqiangScherer, Philipp E.
Issued Date
2014-03
DOI
10.1038/ncomms4485
URI
https://scholarworks.unist.ac.kr/handle/201301/4493
Fulltext
https://www.nature.com/articles/ncomms4485
Citation
NATURE COMMUNICATIONS, v.5, pp.1 - 12
Abstract
We recently identified endotrophin as an adipokine with potent tumour-promoting effects. However, the direct effects of local accumulation of endotrophin in adipose tissue have not yet been studied. Here we use a doxycycline-inducible adipocyte-specific endotrophin overexpression model to demonstrate that endotrophin plays a pivotal role in shaping a metabolically unfavourable microenvironment in adipose tissue during consumption of a high-fat diet (HFD). Endotrophin serves as a powerful co-stimulator of pathologically relevant pathways within the ‘unhealthy’ adipose tissue milieu, triggering fibrosis and inflammation and ultimately leading to enhanced insulin resistance. We further demonstrate that blocking endotrophin with a neutralizing antibody ameliorates metabolically adverse effects and effectively reverses metabolic dysfunction induced during HFD exposure. Collectively, our findings demonstrate that endotrophin exerts a major influence in adipose tissue, eventually resulting in systemic elevation of pro-inflammatory cytokines and insulin resistance, and the results establish endotrophin as a potential target in the context of metabolism and cancer.
Publisher
NATURE PUBLISHING GROUP
ISSN
2041-1723
Keyword
INSULIN-RESISTANCECOLLAGEN-VIOBESE MICECHRONIC INFLAMMATIONTUMOR PROGRESSIONADIPOCYTE DEATHSKELETAL-MUSCLEHYPOXIAEXPRESSIONENDOCRINE

qrcode

Items in Repository are protected by copyright, with all rights reserved, unless otherwise indicated.