There is accumulating evidence that an obesogenic Western diet causes neuroinflammatory damage to the brain, which then promotes further appetitive behaviour. Neuroinflammation has been extensively studied by analysing the translocator protein of 18 kDa (TSPO), a protein that is upregulated in the inflamed brain following a damaging stimulus. As a result, there is a rich supply of TSPO-specific agonists, antagonists and positron emission tomography ligands. One TSPO ligand, etifoxine, is also currently used clinically for the treatment of anxiety with a minimal side-effect profile. Despite the neuroinflammatory pathogenesis of diet-induced obesity, and the translational potential of targeting TSPO, there is sparse literature characterizing the effect of TSPO on appetite. Therefore, in this review, the influence of TSPO on appetite is discussed. Three putative mechanisms for TSPO's appetite-modulatory effect are then characterized: the TSPO–allopregnanolone–GABA_AR signalling axis, glucosensing in tanycytes and association with the synaptic protein RIM-BP1. We highlight that, in addition to its plethora of functions, TSPO is a regulator of appetite. This review ultimately suggests that the appetite-modulating function of TSPO should be further explored due to its potential therapeutic promise.

越来越多的证据表明，导致肥胖的西方饮食会对大脑造成神经炎症损伤，从而促进进一步的食欲行为。神经炎症已通过分析 18 kDa (TSPO) 的转运蛋白进行了广泛研究，TSPO 是一种在受到破坏性刺激后在发炎的大脑中上调的蛋白质。因此，有丰富的 TSPO 特异性激动剂、拮抗剂和正电子发射断层扫描配体供应。一种 TSPO 配体，依替福辛，目前在临床上也用于治疗焦虑症，副作用最小。尽管饮食诱导肥胖的神经炎症发病机制，以及靶向 TSPO 的转化潜力，但很少有文献描述 TSPO 对食欲的影响。因此，在这篇综述中，讨论了 TSPO 对食欲的影响。_一个R 信号轴，单核细胞中的葡萄糖和与突触蛋白 RIM-BP1 的关联。我们强调，除了其过多的功能外，TSPO 还是一种食欲调节剂。这篇综述最终表明，由于其潜在的治疗前景，应进一步探索 TSPO 的食欲调节功能。