ADIPOQ and metabolic syndrome: Visceral adiposity, hyperglycemia, and dyslipidemia contribute to persistent immune activation through distinct pathways, including reduced adiponectin secretion and increased pro-inflammatory cytokine production from adipose tissue, hyperglycemia-promoted oxidative stress and the generation of advanced glycation end products, and stimulation by free fatty acids and oxidized low-density lipoprotein (6, 11, 22).