SLC2A4 and metabolic syndrome: Interestingly, Chen et al. [31] reported that miR-3138 was upregulated in insulin-stimulated human umbilical vein endothelial cells (HUVECs) under a high-glucose environment and linked the deterioration of insulin resistance in the metabolic syndrome with miR-3138 upregulation and KSR2 (kinase suppressor of ras 2)/AMPK (AMP-activated protein kinase)/GLUT4 (glucose transporter isoform 4) signaling repression.