Brain-specific deletion of TRIM13 promotes metabolic stress-triggered insulin resistance, glucose intolerance, and neuroinflammation.

Brain-specific deletion of TRIM13 promotes metabolic stress-triggered insulin resistance, glucose intolerance, and neuroinflammation. Biochem Biophys Res Commun. 2020 Jun 18;527(1):138-145 Authors: Qian Y, Lei G, Wen L Abstract Diabetes has been associated with metabolic disorder, insulin resistance and neuroinflammation. However, the pathogenesis for HFD-induced injury of central nervous system (CNS) is still unclear. Tripartite Motif Containing 13 (TRIM13), also known as RFP2, is a member of TRIM proteins, and is associated with multiple cellular processes, such as apoptosis, survival and inflammation. However, the effects of TRIM13 on brain injury, especially the HFD-induced CNS damage, have not been investigated. To address this issue, the TRIM13flox/flox (fl/fl) mice were produced and then crossed them with Nestin-Cre mice to delete TRIM13 specifically in the brain (cKO). Then, T2D mice with obesity were established by chronic feeding of HFD. We found that brain-specific deletion of TRIM13 accelerated HFD-induced metabolic disorder, insulin resistance and systematic inflammatory response. In addition, HFDcKO mice exhibited significantly higher pro-inflammatory cytokines, including interleukin (IL)-6, IL-1β and tumor necrosis factor-α (TNF-α), in cortex, hippocampus and hypothalamus tissues, which were comparable to the HFDfl/fl mice. Consistently, the activation of nuclear factor-κB (NF-κB) induced by HFD was further aggrav...
Source: Biochemical and Biophysical Research communications - Category: Biochemistry Authors: Tags: Biochem Biophys Res Commun Source Type: research