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10.1038/ncomms14803

http://scihub22266oqcxt.onion/10.1038/ncomms14803
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C5418621!5418621!28466852
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suck abstract from ncbi


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pmid28466852      Nat+Commun 2017 ; 8 (ä): ä
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  • Temporal and tissue-specific requirements for T-lymphocyte IL-6 signalling in obesity-associated inflammation and insulin resistance #MMPMID28466852
  • Xu E; Pereira MMA; Karakasilioti I; Theurich S; Al-Maarri M; Rappl G; Waisman A; Wunderlich FT; Brüning JC
  • Nat Commun 2017[]; 8 (ä): ä PMID28466852show ga
  • Low-grade inflammation links obesity to insulin resistance through the activation of tissue-infiltrating immune cells. Interleukin-6 (IL-6) is a crucial regulator of T cells and is increased in obesity. Here we report that classical IL-6 signalling in T cells promotes inflammation and insulin resistance during the first 8 weeks on a high-fat diet (HFD), but becomes dispensable at later stages (after 16 weeks). Mice with T cell-specific deficiency of IL-6 receptor-? (IL-6R?T-KO) exposed to a HFD display improved glucose tolerance, insulin sensitivity and inflammation in liver and EWAT after 8 weeks. However, after 16 weeks, insulin resistance in IL-6R?T-KO epididymal white adipose tissue (EWAT) is comparable to that of controls, whereas the inflammatory profile is significantly worse. This coincided with a shift from classical T cell IL-6 signalling at 8 weeks, to enhanced IL-6 trans-signalling at 16 weeks. Collectively, our studies reveal that IL-6 action in T cells through classical IL-6 signalling promotes inflammation and insulin resistance early during obesity development, which can be compensated for by enhanced IL-6 trans-signalling at later stages.
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