Abstract:
:Chronic low-grade inflammation is emerging as a pathogenic link between obesity and metabolic disease. Persistent immune activation in white adipose tissue (WAT) impairs insulin sensitivity and systemic metabolism, in part, through the actions of proinflammatory cytokines. Whether obesity engages an adaptive mechanism to counteract chronic inflammation in adipose tissues has not been elucidated. Here we identified otopetrin 1 (Otop1) as a component of a counterinflammatory pathway that is induced in WAT during obesity. Otop1 expression is markedly increased in obese mouse WAT and is stimulated by tumor necrosis factor-α in cultured adipocytes. Otop1 mutant mice respond to high-fat diet with pronounced insulin resistance and hepatic steatosis, accompanied by augmented adipose tissue inflammation. Otop1 attenuates interferon-γ (IFN-γ) signaling in adipocytes through selective downregulation of the transcription factor STAT1. Using a tagged vector, we found that Otop1 physically interacts with endogenous STAT1. Thus, Otop1 defines a unique target of cytokine signaling that attenuates obesity-induced adipose tissue inflammation and plays an adaptive role in maintaining metabolic homeostasis in obesity.
journal_name
Diabetesjournal_title
Diabetesauthors
Wang GX,Cho KW,Uhm M,Hu CR,Li S,Cozacov Z,Xu AE,Cheng JX,Saltiel AR,Lumeng CN,Lin JDdoi
10.2337/db13-1139subject
Has Abstractpub_date
2014-04-01 00:00:00pages
1340-52issue
4eissn
0012-1797issn
1939-327Xpii
db13-1139journal_volume
63pub_type
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