Mitochondrial dysfunction causes inflammatory changes in 3T3-L1 adipocytes

Abstract

   Inflammatory cytokines secreted from adipocytes are known to induce hypertension and insulin resistance resulting in Type 2 diabetes. Mitochondria, which is the keystone of energy metabolism, are continuously controlling cellular states probably including inflammatory states. In this study, we investigated the role of mitochondria on inflammation in 3T3-L1 adipocytes. We cultured 3T3-L1 cells for 17 days after differentiation and treated them with a mitochondrial oxidative phosphorylation uncoupler, FCCP (2 μM in culture medium), for 24 hours. In the cells treated with FCCP, mitochondria appeared to divide and spread away from the lipid droplets. The mRNA expression of TNF-α (tumor necrosis factor-α), IL-6 (Interleukin 6) and MCP-1 (monocyte chemotactic protein 1) in those cells was significantly increased, indicating that mitochondrial dysfunction induced inflammatory changes in 3T3-L1 adipocytes.