Immunometabolism and metainflammation in obesity

Abstract

Recent studies have shown that immune system cells take an active part in the regulation of metabolic homeostasis. Disruption of the interaction between the immune system and metabolic processes makes a major contribution to the current epidemic of a number of non-communicable metabolic diseases. Due to central and peripheral insulin resistance, obesity is closely associated with type 2 diabetes mellitus. Many mechanisms are involved in the genesis of insulin resistance including chronic inflammation in metabolically active tissues (adipose tissue, intestines, muscles, pancreas, liver), as well as in the central nervous system. Potential triggers of obesity-induced metainflammation are cellular hypoxia, mechanical stress of the fat cells, excess of free fatty acids and lypopolysaccharides. Weight loss is a key factor to eliminating inflammation and improving tissue insulin sensitivity. This review presents literature data on the mechanisms of metainflammation in obesity. Taking into account the contribution of metainflammation to the pathogenesis of the disease, the possibilities and prospects of obesity therapy are discussed.