A major contributor to obesity-related pathology is inflammation involving a shift in macrophage polarization toward the inflammatory M1 phenotype and accumulation of such macrophages in the liver and adipose tissue. Activation of Toll-like receptor 4 (TLR4) on macrophages leads the downstream adaptor protein MyD88 to promote M1 polarization through altered gene expression mediated by the transcription factor NF-κB.