Figure 2 Inflammatory pathways affecting hepatic insulin resistance

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Figure 2 Inflammatory pathways affecting hepatic insulin resistance Figure 2 | Inflammatory pathways affecting hepatic insulin resistance. Insulin activates its receptor, which results in tyrosine phosphorylation of insulin receptor substrate (IRS) and activation of downstream effector pathways including the phosphatidylinositol 3-kinase (PI3K)−phosphoinositide-dependent kinase (PDK)−protein kinase B (AKT) and the RAS−extracellular-signal regulated kinase (ERK, also known as mitogen-activated protein kinase) pathways (1). Various pro-inflammatory pathways interfere with insulin signalling either by inhibitory phosphorylation or proteasomal degradation of IRS. High-fat diet, altered microbial composition and reduced intestinal barrier function promote local and systemic inflammation through influx of toll-like receptor ligands. The inhibitor of NF-κB kinase β (IKKβ) represents an important and potent catalyst of insulin resistance besides its role as activator of NF-κB. Numerous pro-inflammatory signalling pathways including TNFα−TNFR1, RANKL–RANK, or IL-1−IL-1R (not shown) activate IKKβ (2). Vast amounts of IL-6 originate from the adipose tissue and promote insulin resistance by inducing suppressor of cytokine signalling (SOCS)1 and 3 via the IL-6R−janus kinase (JAK)3−signal transducer and activator of transcription (STAT)3 axis. SOCS1 and SOCS3 impair insulin signalling through ubiquitin-dependent degradation of IRS (3). c-Jun N-terminal kinase (JNK, also known as mitogen activated protein kinase) represents another important inhibitory kinase of IRS that is activated in response to a variety of extracellular stimuli and cellular stressors such as oxidative and endoplasmic reticulum (ER) stress (4). Pro-inflammatory stimuli are counteracted by adipose-tissue-derived adiponectin via adiponectin receptor (AdipoR)1 and AdipoR2 (5), and by the anti-inflammatory IL-1 family member IL-37 (6) through so far unknown mechanisms. AMPK, 5′-AMP-activated protein kinase; MEK, mitogen-activated protein kinase kinase; PPAR, peroxisome proliferator-activated receptor; ROS, reactive oxygen species; TAB2, TGFβ-activated kinase 1 and MAP3K-binding protein 2; TAK1, mitogen-activated protein kinase kinase kinase 7; TRAF, TNF receptor-associated factor. Tilg, H. et al. (2016) NAFLD and diabetes mellitus Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2016.147