Brown and subcutaneous adipose tissues play a key role in non-shivering thermogenesis both in mice and human, and their activation by adrenergic stimuli promotes energy expenditure, reduces adiposity, and protects against age-related metabolic diseases such as type 2 diabetes (T2D). Low-grade inflammation and insulin resistance characterize T2D. Even though the decline of thermogenic adipose tissues is well-established during ageing, the mechanisms by which this event affects immune system and contributes to the development of T2D is still poorly defined. It is emerging that activation of thermogenic adipose tissues promotes type 2 immunity skewing, limiting type 1 inflammation. Of note, metabolic substrates sustaining type 1 inflammation (e.g. glucose and succinate) are also used by activated adipocytes to promote thermogenesis. Keeping in mind this aspect, a nutrient competition between adipocytes and adipose tissue immune cell infiltrates could be envisaged. Herein, we reviewed the metabolic rewiring of adipocytes during thermogenesis in order to give important insight into the anti-inflammatory role of thermogenic adipose tissues and delineate how their decline during ageing may favor the setting of low-grade inflammatory states that predispose to type 2 diabetes in elderly. A brief description about the contribution of adipokines secreted by thermogenic adipocytes in modulation of immune cell activation is also provided. Finally, we have outlined experimental flow chart procedures and provided technical advices to investigate the physiological processes leading to thermogenic adipose tissue impairment that are behind the immunometabolic decline during aging.
Keywords: Immunity; Inflammation; Metabolism; Nutrient partitioning; Systems Physiology; Type 2 Diabetes.
Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.