Inflammatory Signaling and Brown Fat Activity.

Farah Omran,Mark Christian

doi:10.3389/fendo.2020.00156

Farah Omran, Mark Christian

Open Access

https://doi.org/10.3389/fendo.2020.00156

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Abstract

Obesity is characterized by a state of chronic inflammation in adipose tissue mediated by the secretion of a range of inflammatory cytokines. In comparison to WAT, relatively little is known about the inflammatory status of brown adipose tissue (BAT) in physiology and pathophysiology. Because BAT and brown/beige adipocytes are specialized in energy expenditure they have protective roles against obesity and associated metabolic diseases. BAT appears to be is less susceptible to developing inflammation than WAT. However, there is increasing evidence that inflammation directly alters the thermogenic activity of brown fat by impairing its capacity for energy expenditure and glucose uptake. The inflammatory microenvironment can be affected by cytokines secreted by immune cells as well as by the brown adipocytes themselves. Therefore, pro-inflammatory signals represent an important component of the thermogenic potential of brown and beige adipocytes and may contribute their dysfunction in obesity.

Highlights

Obesity is generally associated with a systemic low-grade inflammation with adipocytes able to produce and release signaling proteins that contribute to this condition [1,2,3,4]
Inflammation has been shown to impact the function of brown AT (BAT) with thermogenic activity inhibited by TNFα-induced insulin resistance and proinflammatory cytokines secreted from macrophages [5,6,7,8]
There is a trade-off between the energetic demands of immunity and homeothermy that permits a hypometabolichypothermic state to favor the immune system

Summary

Introduction

Obesity is generally associated with a systemic low-grade inflammation with adipocytes able to produce and release signaling proteins that contribute to this condition [1,2,3,4]. IL-13, which has anti-inflammatory properties, induces GDF15 (growth differentiation factor 15) expression which is found to protect against obesity by inducing thermogenesis, lipolysis, and oxidative metabolism in mice [112, 113], and prevent inflammation through inhibition of M1 macrophage activation [71]. Deletion of IKKε or IRF3 results in a reduction of inflammatory markers in adipose tissues and enhanced WAT browning with UCP1 expression and energy expenditure increased, while there are only minor effects on BAT [122, 123].

Results

Conclusion