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Immunometabolism and metainflammation in obesity

https://doi.org/10.14341/omet12218

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.

About the Authors

Tatiana R. Romantsova
I.M. Sechenov First Moscow State Medical University
Russian Federation

MD, PhD, professor



Yulia P. Sych
I.M. Sechenov First Moscow State Medical University
Russian Federation

MD, PhD



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Supplementary files

1. Fig. 1. The role of angiogenesis, hypoxia and fibrosis in the genesis of metainflammation of adipose tissue. With healthy expansion of adipose tissue (left), moderate hypoxia induces angiogenesis, moderate accumulation of immune cells and reorganization of the intracellular matrix to prevent lipid ectopia in lean tissues. In obesity (right), excessive adipocyte hypertrophy leads to severe hypoxia, impaired angiogenesis, extracellular matrix fibrosis, adipose tissue infiltration by pro-inflammatory macrophages (adapted from C. Crewe et al., 2017 [14]).
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2. Fig. 2. Inflammation in skeletal muscle in obesity. A. Healthy muscles contain a small amount of immune cells. B. With obesity, an expansion of intramuscular adipose tissue (intermyocytic and perimyocytic) develops. Immune cells (macrophages, T-lymphocytes) infiltrate intramuscular adipose tissue, which leads to muscle inflammation. In conditions of inflammation, myocytes express cytokines and chemokines. B. The pro-inflammatory cytokines and chemokines produced by myocytes, adipocytes and immune cells, along with free fatty acids, accumulate intramuscularly, causing a progression in the recruitment of immune cells and forming a self-sustaining vicious cycle of inflammation (adapted from H. Wu, Ch. M. Ballantyne, 2017 [ 27]).
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3. Fig. 3. The role of resident intra-island macrophages in glucose homeostasis. Obesity in mice is associated with the expansion of intra-island CD11c + macrophages, which capture insulin vesicles and interfere with its secretion by the pancreas. Periostrovular and isletic macrophages control the function of β-cells and glucose homeostasis (adapted from O. Spadaro, V.D. Dixit, 2019 [36]).
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4. Fig. 4. The contribution of central nervous system cells to the pathogenesis of hypothalamic inflammation (adapted from A. Jais, J.B. Brüning, 2017 [49]).
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Review

For citations:


Romantsova T.R., Sych Yu.P. Immunometabolism and metainflammation in obesity. Obesity and metabolism. 2019;16(4):3-17. (In Russ.) https://doi.org/10.14341/omet12218

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