Fig. 1

Mechanisms underlying uric acid (UA)-induced β-cell dysfunction. UA probably enters the β-cells via glucose transporter 9 (GLUT9). Intracellular UA increases reactive oxygen species (ROS), which phosphorylates and activates AMP-activated protein kinase (AMPK) and then extracellular signal-regulated kinase (ERK). Phosphorylated ERK causes β-cell apoptosis. UA also phosphorylates and degrades inhibitor of kappa B (IκB) that permits the transcription factor nuclear factor kappa B (NF-κB) to enter the nucleus and increases expression of inducible nitric oxide synthase (iNOS). NO overproduction decreases glucose-stimulated insulin secretion (GSIS) and causes β-cell apoptosis. CXCL-1, chemokine (C-X-C motif) ligand 1; MCP-1, monocyte chemoattractant protein-1; IL-6, interleukin-6. Created with BioRender.com