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.

棕色和皮下脂肪组织在小鼠和人类的非颤抖性产热中起着关键作用，肾上腺素能刺激它们的激活可促进能量消耗，减少肥胖，并预防与年龄有关的代谢性疾病，如2型糖尿病（T2D）。低度炎症和胰岛素抵抗是T2D的特征。即使在衰老过程中已经很好地确定了生热脂肪组织的下降，但该事件影响免疫系统并促进T2D发生的机制仍然不清楚。新兴的产热脂肪组织的激活促进2型免疫倾斜，限制了1型炎症。值得注意的是，活化的脂肪细胞也使用维持1型炎症的代谢底物（例如葡萄糖和琥珀酸酯）来促进生热。牢记这一方面，可以设想脂肪细胞和脂肪组织免疫细胞浸润之间的营养竞争。本文中，我们综述了生热过程中脂肪细胞的代谢重建，以便对生热脂肪组织的抗炎作用提供重要见解，并描述它们在衰老过程中的下降如何可能有助于易患2型糖尿病的低度炎症状态在老年人中。还简要介绍了产热脂肪细胞分泌的脂肪因子在调节免疫细胞活化中的作用。最后，我们概述了实验流程图程序并提供了技术建议，以研究导致衰老过程中免疫代谢下降的热源脂肪组织损伤的生理过程。可以设想脂肪细胞与脂肪组织免疫细胞浸润之间的营养竞争。本文中，我们综述了生热过程中脂肪细胞的代谢重建，以便对生热脂肪组织的抗炎作用提供重要见解，并描述它们在衰老过程中的下降如何可能有助于易患2型糖尿病的低度炎症状态在老年人中。还简要介绍了产热脂肪细胞分泌的脂肪因子在调节免疫细胞活化中的作用。最后，我们概述了实验流程图程序并提供了技术建议，以研究导致衰老过程中免疫代谢下降的热源脂肪组织损伤的生理过程。可以设想脂肪细胞与脂肪组织免疫细胞浸润之间的营养竞争。本文中，我们综述了生热过程中脂肪细胞的代谢重建，以便对生热脂肪组织的抗炎作用提供重要见解，并描述它们在衰老过程中的下降可能如何促进易患2型糖尿病的低度炎症状态的发生。在老年人中。还简要介绍了产热脂肪细胞分泌的脂肪因子在调节免疫细胞活化中的作用。最后，我们概述了实验流程图程序并提供了技术建议，以研究导致衰老过程中免疫代谢下降的热源脂肪组织损伤的生理过程。