Fig. 1. Hypothesis for a mechanism by which excess glucose and saturated free fatty acids (SFAs) affect reactive oxygen species (ROS) generation in adipocytes in early stages of obesity. Excess glucose generates ROS via the pentose phosphate pathway, rather than by overloading mitochondrial oxidative phosphorylation, while SFA generate ROS following activating, Toll-like receptor 4 (TLR4) or lipid rafts. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX4) might be the common mediator of ROS generation by both excess glucose and SFAs. ROS generated by both glucose and SFA activate nuclear factor κB (NF-κB). LR, lipid raft; SAA3, serum amyloid A3; MCP-1, monocyte chemoattractant protein-1.
