NFKB1 and Hyperglycemia: Experimental paradigms involving longer (e.g., 8-24 hour) exposures to hyperglycemia or palmitate suggest that these stressors can also induce changes in gene expression or post-transcriptional modifications, including suppression of AMPK signaling and induction of NFκ-B mediated pro-inflammatory signaling, that may act to suppress endothelial function [52, 84–86].