Figure 8.

A proposed model of adipocyte fatty acid-binding protein (A-FABP)-mediated mitochondrial dysfunction and apoptosis induced by palmitate (PA) in macrophages. High exposure of PA leads to oxidative stress, indicated by excessive reactive oxidative species (ROS) generation originated from electron leakage of respiratory chain and subsequent lipid perioxidation. PA causes impaired mitochondrial biogenesis including reduced mitochondrial number and expression of mitochondrial biogenesis-related protein PPARγ coactivator 1-α. Mitochondrial function is also widespreadly compromised by PA as indicated by impaired adenosine triphosphate (ATP) generation, downregulated Δψm, and cytochrome c release. All of these eventually result in macrophage apoptosis through the activation of caspase 3. The inhibition of A-FABP with BMS309403 protects against mitochondrial dysfunction and apoptosis induced by PA.