Immune regulation in obesity: a narrative review

Abstract

Obesity is a condition triggered by many risk factors, but the main one is due to high calorie intake and low physical activity. Various studies have explored the relationship between obesity and metabolic complications, namely chronic degenerative disorders. In the condition of obesity, there are biochemical changes including chronic inflammation. This condition mainly occurs due to the load on the metabolic tissue due to weight gain and fat tissue dysfunction. These changes result in changes in the distribution of leukocytes, lymphocyte activity, and in general the immune defense system. The changes that occur include the occurrence of a chronic inflammatory process. Among the various inflammatory mediators, there are three mediators that play an important role in the regulation of the immune system due to obesity, namely TNF-α, IL-6, and adiponectin. In addition, the accumulation of free fatty acids in obesity can activate a cascade of a series of pro-inflammatory kinases, such as IkB kinase and c-Jun N-terminal kinase, which triggers fatty tissue to release IL-6. Other effects include activation of the inflammasome, and hyperleptinemia. Leptin is then associated with cell survival, cytokine release, and chemotaxis. In addition, leptin can also be related to the proliferation of T cells.