Fig. 5.

Mechanism underlying visceral adipose tissue IR induced by periodontitis-derived virulence factors. Virulence factors can mediate oxidative stress, activate macrophages to induce inflammatory responses, and disrupt specific adipokine secretion, resulting in visceral adipose tissue IR. Black arrows represent activating events; red arrows represent inhibitory events. TLRs Toll-like receptors, AP antigen presentation, RBP4 retinol-binding protein 4, Nrf2 nuclear factor erythroid-2 related factor 2, NOX2 NADPH oxidase 2, NOX4 NADPH oxidase 4, iNOS inducible nitric oxide synthase, MnSOD manganese superoxide dismutase, HO-1 heme oxygenase-1, ROS reactive oxygen species, IRS insulin receptor substrate, HSL hormone-sensitive lipase, TAG triacylglycerol, TNF-α tumor necrosis factor-α, TNFR tumor necrosis factor receptor, IL-1β interleukin-1β, IL-1R IL-1 receptor, NF-κB nuclear factor kappa-B, PPARγ peroxisome proliferator-activated receptor γ, IR insulin resistance, ERS endoplasmic reticulum stress, LepRb leptin receptor, JAK2 Janus kinase 2, SOCS-3 suppressor of cytokine signaling-3, Akt protein kinase B, LFA-1 lymphocyte function-associated antigen-1, GLUT4 glucose transporter 4