在小鼠癌症恶病质期间，S100A8/A9复合物促进食物摄入并防止脂肪组织损失，这一成果由中国科学院深圳先进技术研究院John R. Speakman研究小组经过不懈努力而取得。相关论文发表在2026年3月3日出版的《细胞—代谢》杂志上。

研究团队发现下丘脑中的S100钙结合蛋白A8和A9（S100A8/A9）和补体3（C3）在癌症恶病质期间减少食物摄入和脂肪量中起关键作用。外周给药S100A8/A9抑制剂和下丘脑敲低C3显著增加食物摄入量，部分恢复脂肪和瘦肉组织的损失。

据介绍，癌症恶病质是一种消耗综合征，其特征是食物摄入量减少，瘦肉和脂肪组织减少。在小鼠中，癌症恶病质涉及宿主脂肪和瘦肉质量（特别是骨骼肌）的显著减少，这与肿瘤生长相平衡。利用¹⁵N示踪，肿瘤从食物摄入和宿主组织分解中获得蛋白质（氮）。由于肿瘤、棕色脂肪组织（BAT）和其他器官之间的代谢补偿，总能量消耗保持不变，这一现象在癌症患者中也观察到。脂肪减少导致的瘦素减少并没有刺激食物摄入或减少能量消耗。

附：英文原文

Title: The S100A8/A9 complex promotes food intake and prevents adipose tissue loss during cancer cachexia in mice

Author: Lin Gao, Ying Liu, Ying Yu, Yingga Wu, Huanan Zhang, Cui Wang, Xinrui Gao, Yang Chen, Tingjie Zhang, Sixian Huang, Zhonghui Zhang, Zengguang Jin, Jie Chen, Haiyang Jing, Dehuang Kong, Yanlin Tian, Jacques Togo, Yong Lei, Yi Huang, Fan Xia, Min Li, Anyongqi Wang, Chao Jia, Sumei Hu, Di Chen, Xina Xie, Lu Wang, Jie Liu, Xiaomeng Wu, Changyong Tang, Chaoqun Niu, Zesong Li, John R. Speakman

Issue&Volume: 2026-03-03

Abstract: Cancer cachexia is a wasting syndrome characterized by reduced food intake and lean and fat tissue loss. In mice, cancer cachexia involved marked reductions in host fat and lean mass (particularly skeletal muscle), which were balanced by tumor growth. Using 15N tracing, the tumor gets protein (nitrogen) from both food intake and host tissue breakdown. Total energy expenditure remained unchanged due to metabolic compensation among the tumor, brown adipose tissue (BAT), and other organs, a phenomenon also observed in people with cancer. The decrease in leptin caused by fat loss did not stimulate food intake or reduce energy expenditure. We show that S100 calcium-binding protein A8 and A9 (S100A8/A9) and complement 3 (C3) in the hypothalamus play a key role in the reduction of food intake and fat mass during cancer cachexia. The peripheral administration of S100A8/A9 inhibitors and the hypothalamic knockdown of C3 significantly increased food intake and partially rescued fat and lean tissue loss.

DOI: 10.1016/j.cmet.2026.02.005

Source: https://www.cell.com/cell-metabolism/abstract/S1550-4131(26)00048-3