Figure 4

Inflammatory metabolic syndrome. This schematic summarises the key inflammatory stimuli arising from excessive nutrient intake, the main tissues experiencing inflammatory changes, the predominant inflammatory mediator output of these tissues and the impact of these changes on propagation of the metabolic syndrome and associated risk for Alzheimer’s disease. In particular it has emerged that hypothalamic inflammation produces hypothalamic dysfunction, which further disrupts central nervous system regulation of appetite and energy expenditure. Dashed arrows indicate that though these mediators are the result of inflammatory stimulation in the tissues/joints, they also contribute to the ongoing inflammation in those tissues. AGE, advanced glycation end products; CRP, C reactive protein; ER, endoplasmic reticulum stress; FFA, free fatty acids; IL, interleukin; LDL, low density lipoprotein; NO, nitric oxide; ROS, reactive oxygen species; tumour necrosis factor.