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Park, Jiyoung
Molecular Metabolism Laboratory (MML)
Research Interests
  • Obesity, diabetes, adipose tissue, cancer, cancer-associated adipocyte, dermal adipocyte, metabolic memory

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Endotrophin triggers adipose tissue fibrosis and metabolic dysfunction

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Title
Endotrophin triggers adipose tissue fibrosis and metabolic dysfunction
Author
Sun, KaiPark, JiyoungGupta, Olga T.Holland, William L.Auerbach, PernilleZhang, NingyanMarangoni, Roberta GoncalvesNicoloro, Sarah M.Czech, Michael P.Varga, JohnPloug, ThorkilAn, ZhiqiangScherer, Philipp E.
Keywords
INSULIN-RESISTANCE; COLLAGEN-VI; OBESE MICE; CHRONIC INFLAMMATION; TUMOR PROGRESSION; ADIPOCYTE DEATH; SKELETAL-MUSCLE; HYPOXIA; EXPRESSION; ENDOCRINE
Issue Date
201403
Publisher
NATURE PUBLISHING GROUP
Citation
NATURE COMMUNICATIONS, v.5, no., 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.
URI
http://scholarworks.unist.ac.kr/handle/201301/4493
DOI
http://dx.doi.org/10.1038/ncomms4485
ISSN
2041-1723
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