Chronic Inflammation in Obesity and the Metabolic Syndrome

The increasing incidence of obesity and the metabolic syndrome is disturbing. The activation of inflammatory pathways, used normally as host defence response, reminds us of the seriousness of this condition. There is most probably more than one cause for the activation of inflammation, a timeline of events related to the deterioration of metabolic homeostasis presenting along variable routes. Apparently, metabolic overload evokes several stress reactions, such as oxidative, inflammatory, organelle, and cell hypertrophy stresses, generating vicious cycles that amplify each other leading to dysfunction. Adipocyte hypertrophy, through purely physical reasons, facilitates cell rupture, what will evoke an inflammatory reaction. Inability of adipose tissue development to engulf all incoming fat leads to fat deposition in other organs, mainly in the liver, with marked consequences on insulin resistance. The oxidative stress which accompanies feeding, particularly when there is an excessive ingestion of fat and/or other macronutrients without concomitant ingestion of antioxidant-rich foods/beverages, may contribute to the inflammatory markers attributed to obesity. Moreover, recent data on the microbiota and its interaction with food and with obesity brought new hypothetic mechanisms for the obesity/fat diet relationship with inflammation. Beyond these common confounders, other phenomena, for instance, psychological and/or circadian rhythm disturbances, may likewise contribute to the raise of oxidative/inflammatory status. The difficulty in the management of the obesity/metabolic syndrome pathologies is linked to their multifactorial nature where environmental, genetic, and psychosocial factors interact through highly complex networks.