The overwhelming prevalence of obesity is a priority for public health compromising human lifespan and representing important economic burden worldwide. Obesity is characterized by a state of chronic low-grade inflammation associated to metabolic dysfunction. Although the efforts for unravelling the complex immunometabolic signaling pathways to explain the association of obesity with type 2 diabetes, cardiovascular diseases, cancer, neurodegenerative diseases and psychiatric disorders, we still do not have all the picture to design effective therapeutic to fight these immunometabolic disease clusters. Dopaminergic pathways apart from having a major role in the regulation of appetite and feeding behaviors are important immunoregulators in inflammation; thus, dopaminergic regulation is suggested to impact obesity- associated inflammation. Dopamine (DA) has been reported to modulate immune function and immune cells themselves produce endogenous DA. DA-induced immunomodulation is currently the focus of intense experimental research and dopaminergic pathways are increasingly considered a target for drug development in immune diseases. While the role of dopaminergic pathways in immune-mediated diseases has been intensively investigated in neurodegenerative diseases, dopaminergic immunomodulation in obesity-associated inflammation is largely unknown. This review will integrate the actual knowledge about dopaminergic pathways involved in obesity-associated inflammation with special focus on immune innate key cell players. We present an explanatory hypothesis with a model that integrate central and peripheral dopaminergic circuits in the relationship between neuroimmune and metabolic systems in obesity-associated inflammation. A perspective on the potential role of dopaminergic drugs in the context of obesity will be given.

Graphical representation of central and peripheral dopaminergic pathways in obesity-associated inflammation

中文翻译：

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肥胖相关炎症中的多巴胺能途径。

肥胖症的普遍流行是危害人类寿命并代表着全球范围内重要经济负担的公共卫生工作的重中之重。肥胖的特征在于与代谢功能障碍相关的慢性低度炎症状态。尽管努力阐明复杂的免疫代谢信号通路来解释肥胖与2型糖尿病，心血管疾病，癌症，神经退行性疾病和精神疾病的关系，但我们仍然没有全部图景来设计有效的治疗方法来对抗这些免疫代谢性疾病。多巴胺能途径除了在食欲和进食行为的调节中起主要作用外，在炎症中也是重要的免疫调节剂。因此，建议多巴胺能调节影响肥胖相关的炎症。据报道，多巴胺（DA）可调节免疫功能，免疫细胞本身可产生内源性DA。DA诱导的免疫调节目前是大量实验研究的重点，而多巴胺能途径越来越被认为是免疫疾病中药物开发的目标。尽管已经在神经退行性疾病中深入研究了多巴胺能途径在免疫介导疾病中的作用，但在肥胖相关炎症中的多巴胺能免疫调节仍是未知的。这篇综述将整合有关与肥胖相关的炎症相关的多巴胺能途径的实际知识，并特别关注免疫先天关键细胞参与者。我们提出了一个模型的解释性假设，该模型整合了肥胖相关炎症中神经免疫系统和代谢系统之间的关系中的中央和外围多巴胺能回路。将给出关于多巴胺能药物在肥胖中的潜在作用的观点。

肥胖相关炎症中中央和外周多巴胺能途径的图形表示