TonEBP suppresses adipogenesis and insulin sensitivity by blocking epigenetic transition of PPARγ2.

Citation data:

Scientific reports, ISSN: 2045-2322, Vol: 5, Issue: 1, Page: 10937

Publication Year:
2015
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Repository URL:
http://scholarworks.unist.ac.kr/handle/201301/17541
PMID:
26042523
DOI:
10.1038/srep10937
PMCID:
PMC4455245
Author(s):
Lee, Jun Ho; Lee, Hwan Hee; Ye, Byeong Jin; Lee-Kwon, Whaseon; Choi, Soo Youn; Kwon, Hyug Moo
Publisher(s):
Springer Nature; NATURE PUBLISHING GROUP
Tags:
Multidisciplinary; TRANSCRIPTION FACTOR NFAT5; ENHANCER-BINDING PROTEIN; PPAR-GAMMA EXPRESSION; ADIPOSE-TISSUE; ADIPOCYTE DIFFERENTIATION; METABOLICALLY HEALTHY; NUCLEAR-FACTOR; OBESITY; INFLAMMATION; RESISTANCE
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article description
TonEBP is a key transcription factor in cellular adaptation to hypertonic stress, and also in macrophage activation. Since TonEBP is involved in inflammatory diseases such as rheumatoid arthritis and atherosclerosis, we asked whether TonEBP played a role in adipogenesis and insulin resistance. Here we report that TonEBP suppresses adipogenesis and insulin signaling by inhibiting expression of the key transcription factor PPARγ2. TonEBP binds to the PPARγ2 promoter and blocks the epigenetic transition of the locus which is required for the activation of the promoter. When TonEBP expression is reduced, the epigenetic transition and PPARγ2 expression are markedly increased leading to enhanced adipogenesis and insulin response while inflammation is reduced. Thus, TonEBP is an independent determinant of adipose insulin sensitivity and inflammation. TonEBP is an attractive therapeutic target for insulin resistance in lieu of PPARγ agonists.