Toll-like receptor, lipotoxicity and chronic inflammation: the pathological link between obesity and cardiometabolic disease.
The epidemic growth in the prevalence of obesity has made the impact of metabolic syndrome on cardiovascular events increasingly significant. Elevated visceral adiposity, the indispensable component of metabolic syndrome, is thought to play a primary role in the increasing incidence of cardiometabolic disorders. Importantly, obesity is not merely the simple expansion of adipose tissue mass; it also involves the activation of inflammatory processes within visceral adipose tissue. Adipose tissue inflammation on the one hand enhances the production of proinflammatory adipokines and on the other hand increases the release of free fatty acids via the activation of lipolysis. The adipokines and free fatty acids secreted from visceral fat then contribute to a cardiometabolic pathology. We herein summarize recent advances in our understanding of the mechanisms by which visceral obesity leads to the activation of inflammation in cardiovascular and metabolic tissues and promotes cardiometabolic disease. Our focus is on Toll-like receptor 4 signaling and free fatty acids as mediators of chronic inflammation in patients with metabolic syndrome and atherosclerosis.
Department of Cardiovascular Medicine, The University of Tokyo.
Kosei
K
Eguchi
Ichiro
I
Manabe
D050154:Adiposity; D000818:Animals; D006331:Heart Diseases / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology*; D052439:Lipid Metabolism Disorders / Q000378:metabolism / Q000473:pathology*; D024821:Metabolic Syndrome / Q000378:metabolism / Q000473:pathology*; D009765:Obesity / Q000378:metabolism / Q000473:pathology*; D051193:Toll-Like Receptors / Q000378:metabolism*
D051193:Toll-Like Receptors