中国儿童保健杂志 ›› 2025, Vol. 33 ›› Issue (10): 1052-1055.DOI: 10.11852/zgetbjzz2025-0969

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多系统交互网络视角下儿童肥胖相关代谢性疾病的免疫-代谢-力学三维机制解析

郭锡熔   

  1. 上海市同仁医院,上海交通大学医学院附属同仁医院,虹桥国际医学研究院,上海 200336
  • 收稿日期:2025-08-26 修回日期:2025-08-30 发布日期:2025-10-11
  • 通讯作者: 郭锡熔,E-mail:xrguo@shsmu.edu.cn
  • 作者简介:郭锡熔(1966—),男,主任医师,博士生导师,主要研究方向为儿童肥胖与代谢综合征。
  • 基金资助:
    国家重点研发计划(2021YFC2701900, 2021YFC2701903);国家自然科学基金(82170869)

Three-dimensional mechanisms of immune-metabolic-mechanical interactions in metabolic diseases associated with childhood obesity from the perspective of multi-system interaction networks

GUO Xirong   

  1. Hongqiao International Institute of Medicine, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200336, China
  • Received:2025-08-26 Revised:2025-08-30 Published:2025-10-11
  • Contact: GUO Xirong,E-mail:xrguo@shsmu.edu.cn

摘要: 儿童肥胖及相关代谢性疾病(如胰岛素抵抗、脂代谢紊乱、代谢相关脂肪性肝病等)已成为重要公共卫生问题。既往研究往往聚焦于单一器官或组织层面的改变,难以解析肥胖进程中多组织器官的动态变化。儿童肥胖相关代谢紊乱本质上是脂肪组织功能障碍引发的、涉及免疫系统失调和代谢稳态失衡等多系统深度交互的复杂网络性疾病。本文系统综述了当前儿童肥胖与代谢性疾病之间关联机制的研究进展,重点聚焦三大病理路径:免疫细胞介导的慢性炎症、代谢物积累与代谢重编程、以及脂肪组织生物力学微环境异常。研究显示,在肥胖状态下,T细胞、B细胞及巨噬细胞在脂肪组织中活性改变,构建免疫-代谢的双向反馈回路;支链氨基酸和非酯化脂肪酸等代谢物可干扰胰岛素信号传导,引发胰岛素抵抗;而细胞外基质硬化及力学应激增强则进一步激活炎症通路,形成“免疫-代谢-基质”复合网络。儿童肥胖相关代谢异常具有早发、多器官、长期遗留等特点。未来应加强多组学技术整合与多系统互作机制研究,推动个体化干预策略的临床转化,以改善儿童肥胖相关代谢疾病的防治效果。

关键词: 儿童肥胖, 代谢性疾病, 免疫细胞, 代谢重编程, 细胞生物力学

Abstract: Childhood obesity and its associated metabolic diseases (e.g., insulin resistance, dyslipidemia, metabolic dysfunction-associated fatty liver disease, etc.) have emerged as a significant public health concern.Previous studies often focused on changes at the single organ or tissue level, making it challenging to elucidate the dynamic changes across multiple tissues and organs during the progression of obesity.Metabolic disorders related to childhood obesity are essentially complex network diseases initiated by the dysfunction or collapse of adipose tissue function, involving deep interactions among multiple systems such as immune system dysregulation and the collapse of metabolic homeostasis.This study systematically reviews current research progress on the mechanisms underlying the association between childhood obesity and metabolic diseases, with a focus on three key pathological pathways: chronic inflammation mediated by immune cells, metabolite accumulation and metabolic reprogramming, and abnormal changes in adipose tissue biomechanics microenvironment.It is reported that T cells, B cells, and macrophages exhibit altered activity in adipose tissue with obesity, establishing a bidirectional feedback loop between immunity and metabolism.Metabolites such as branched-chain amino acids and non-esterified fatty acids can interfere with insulin signaling, inducing insulin resistance.Besides, extracellular matrix stiffening and increased mechanical stress further activate inflammatory pathways, forming an immune-metabolic-matrix composite network.Metabolic abnormalities associated with childhood obesity are characterized by early onset, multi-organ involvement, and long-term persistence.Future research should enhance the integration of multi-omics technologies with investigations into the mechanisms of multi-system interactions, promoting the clinical translation of personalized intervention strategies, and thereby improving the prevention and treatment outcomes of childhood obesity-related metabolic diseases.

Key words: childhood obesity, metabolic diseases, immune cells, metabolic reprogramming, cellular biomechanics

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