Obese IL-1 receptor-I-deficient (IL-1RI−/−) mice are protected against diet-induced insulin resistance via a down-regulation of inflammation and oxidative stress in adipose tissue: a proteomics investigation

IL-1RI-/- mice also showed lower levels of various isoforms of proteasomes and ubiquitin ligase, which may suggest a down-regulation of the inflammatory response in EAT via decreased ubiquitination and proteasomal degradation of inhibitory subunit of NF-κB, and increased suppression of the key inflammatory transcription factor NF-κB. Furthermore, IL-1RI-/- mice had decreased expression of a host of cytoskeletal proteins, which may reflect apoptosis and cytoskeletal remodelling in EAT, possibly as a result of cell death of macrophages and monocytes.