The incidence of depression and anxiety is amplified by obesity. Mounting evidence reveals that the psychiatric consequences of obesity stem from poor diet, inactivity, and visceral adipose accumulation. Resulting metabolic and vascular dysfunction, including inflammation, insulin and leptin resistance, and hypertension, have emerged as key risks to depression and anxiety development. Recent research advancements are exposing the important contribution of these different corollaries of obesity and their impact on neuroimmune status and the neural circuits controlling mood and emotional states. Along these lines, this review connects the clinical manifestations of depression and anxiety in obesity to our current understanding of the origins and biology of immunometabolic threats to central nervous system function and behavior.

肥胖加剧了抑郁症和焦虑症的发病率。越来越多的证据表明，肥胖的精神后果源于不良饮食、不运动和内脏脂肪堆积。由此产生的代谢和血管功能障碍，包括炎症、胰岛素和瘦素抵抗以及高血压，已成为抑郁和焦虑发展的主要风险。最近的研究进展揭示了肥胖这些不同推论的重要贡献及其对神经免疫状态和控制情绪和情绪状态的神经回路的影响。沿着这些思路，这篇综述将肥胖症中抑郁和焦虑的临床表现与我们目前对免疫代谢威胁对中枢神经系统功能和行为的起源和生物学的理解联系起来。