Abstract
Obesity-associated insulin resistance is accompanied by an alteration in the Th1/Th2 balance in adipose tissue. T-bet (Tbx21) is an immune cell transcription factor originally described as the master regulator of Th1 cell development, although is now recognized to have a role in both the adaptive and innate immune systems. T-bet also directs T-cell homing to pro-inflammatory sites by the regulation of CXCR3 expression. T-bet−/− mice have increased visceral adiposity but are more insulin-sensitive, exhibiting reduced immune cell content and cytokine secretion specifically in the visceral fat depot, perhaps due to altered T-cell trafficking. Studies of T-bet deficiency on Rag2- and IFN-γ-deficient backgrounds indicate the importance of CD4+ T cells and IFN-γ in this model. This favorable metabolic phenotype, uncoupling adiposity from insulin resistance, is present in young lean mice yet persists with age and increasing obesity. We suggest a novel role for T-bet in metabolic regulation.
| Original language | English |
|---|---|
| Article number | N/A |
| Pages (from-to) | 58-62 |
| Number of pages | 50 |
| Journal | Adipocyte |
| Volume | 3 |
| Issue number | 1 |
| Early online date | 28 Aug 2013 |
| DOIs |
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| Publication status | Published - Jan 2014 |