Cellular and molecular overview of gestational diabetes mellitus: Is it predictable and preventable?

Figure 4 Brief summary of the nuclear factor-kappa B signaling pathway. As suppressors, the inhibitory regulators of nuclear factor-kappa B (NF-κB) can bind to the NF-κB dimers to form a complex, which remains sequestered and inactive in the cytoplasm of non-stimulated cells. Under the status of insulin resistance, proinflammatory cytokines (IL-1β, IL-6, and TNFα) and toll-like receptors are increased to initiate the phosphorylation and degradation of inhibitory regulators of NF-κB to expose a nuclear localization sequence on the NF-κB proteins. Thus, the NF-κB dimers translocate to the nucleus to regulate gene transcription and induce inflammatory cascades. IκB: Inhibitory regulators of nuclear factor-kappa B; TLR: Toll-like receptor.