Cell metabolism最新文献

Weight loss during intermittent fasting, not Mediterranean diet quality alone, is associated with lower inflammation: A randomized controlled trial 一项随机对照试验表明，间歇性禁食期间的体重减轻与较低的炎症有关，而不仅仅是地中海饮食质量

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-21 DOI: 10.1016/j.cmet.2026.09.017

Moritz V. Warmbrunn,Valeria Tosti,Raaj Kishore Biswas,Beatrice Bertozzi,Maria Lastra Cagigas,Nicola Veronese,Francesco Spelta,Laura Piccio,Richard D. Head,Richard R. Rodrigues,Dayna S. Early,Yanjiao Zhou,Giorgio Trinchieri,Giovanni Fiorito,Luigi Fontana

{"title":"Weight loss during intermittent fasting, not Mediterranean diet quality alone, is associated with lower inflammation: A randomized controlled trial","authors":"Moritz V. Warmbrunn,Valeria Tosti,Raaj Kishore Biswas,Beatrice Bertozzi,Maria Lastra Cagigas,Nicola Veronese,Francesco Spelta,Laura Piccio,Richard D. Head,Richard R. Rodrigues,Dayna S. Early,Yanjiao Zhou,Giorgio Trinchieri,Giovanni Fiorito,Luigi Fontana","doi":"10.1016/j.cmet.2026.09.017","DOIUrl":"https://doi.org/10.1016/j.cmet.2026.09.017","url":null,"abstract":"Whether the anti-inflammatory effects of a Mediterranean diet reflect diet quality itself or accompanying weight loss is unclear. In a 16-week randomized controlled-feeding trial, 53 adults (77% female; mean age 54.7 years) with metabolic risk factors received a fully provided Mediterranean diet or their habitual western diet for 8 weeks, then added twice-weekly fasting days for a further 8 weeks. The primary outcome, high-sensitivity C-reactive protein, did not change during the diet-only phase despite clear dietary separation. After fasting began, C-reactive protein fell in the Mediterranean-diet group relative to controls, alongside greater weight loss, improved insulin sensitivity, and lower blood pressure; lipid improvements had already emerged during the diet-only phase. Multi-omic analyses showed parallel reductions in inflammatory signaling, with gut microbiome composition largely stable. Thus, diet quality alone does not lower inflammation over 8 weeks; negative energy balance and weight loss during fasting appear to be the stronger drivers. This study was registered at ClinicalTrials.gov (NCT02148458).","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"3 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Propionate promotes MHC class I antigen presentation and anti-tumor immunity 丙酸促进MHC I类抗原呈递和抗肿瘤免疫

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-21 DOI: 10.1016/j.cmet.2026.09.018

Suyao Li,Dong Guo,Qingqing Yang,Yizhi Cao,Yu Dong,Xiaoming Jiang,Xinyao Tian,Dou Nie,Lihui Wu,Qingang Wu,Xuxiao He,Yanyan Hu,Rongxuan Zhu,Ning Zhu,Shudi Luo,Yinan Shen,Yuhao Wang,Zhexu Chi,Ying Yuan,Daqian Xu,Weilin Wang,Yuan Ding,Zhimin Lu

{"title":"Propionate promotes MHC class I antigen presentation and anti-tumor immunity","authors":"Suyao Li,Dong Guo,Qingqing Yang,Yizhi Cao,Yu Dong,Xiaoming Jiang,Xinyao Tian,Dou Nie,Lihui Wu,Qingang Wu,Xuxiao He,Yanyan Hu,Rongxuan Zhu,Ning Zhu,Shudi Luo,Yinan Shen,Yuhao Wang,Zhexu Chi,Ying Yuan,Daqian Xu,Weilin Wang,Yuan Ding,Zhimin Lu","doi":"10.1016/j.cmet.2026.09.018","DOIUrl":"https://doi.org/10.1016/j.cmet.2026.09.018","url":null,"abstract":"Defective tumor antigen presentation promotes immune evasion and resistance to immune checkpoint blockade. Here, we identified the short-chain fatty acid propionate as a potent enhancer of major histocompatibility complex class I (MHC class I) antigen presentation. Propionate stabilizes MHC class I on tumor cells, promotes CD8+ T cell infiltration and activation, and suppresses tumor growth. Mechanistically, the E3 ubiquitin (Ub) ligase STUB1 directly interacts with human leukocyte antigen (HLA)-A to mediate K168/K170 polyubiquitination and subsequent degradation. Propionate directly binds STUB1 through hydrogen bonds involving K30 and N34, residues that overlap with the MHC class I-binding interface. This interaction blocks STUB1-mediated MHC class I polyubiquitination, thereby stabilizing MHC class I, enhancing T cell receptor (TCR) engagement and T cell activation, and restraining tumor growth. Importantly, propionate or the propionate-producing probiotic Akkermansia muciniphila markedly enhanced anti-PD-1 efficacy. These findings uncover a non-metabolic moonlighting function of short-chain fatty acids in regulating tumor immunity and provide a rationale for leveraging dietary propionate or propionate-producing probiotics to enhance immune checkpoint therapy.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"12 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2026-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149225922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A context-dependent framework for targeting NAD metabolism in cancer 针对癌症中NAD代谢的上下文依赖框架

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-15 DOI: 10.1016/j.cmet.2026.09.015

Leire Arrizabalaga,Laura Santambrogio,Guido Kroemer,Lorenzo Galluzzi,Aitziber Buqué

{"title":"A context-dependent framework for targeting NAD metabolism in cancer","authors":"Leire Arrizabalaga,Laura Santambrogio,Guido Kroemer,Lorenzo Galluzzi,Aitziber Buqué","doi":"10.1016/j.cmet.2026.09.015","DOIUrl":"https://doi.org/10.1016/j.cmet.2026.09.015","url":null,"abstract":"Nicotinamide adenine dinucleotide (NAD) occupies a privileged position at the intersection of cellular bioenergetics, redox homeostasis, and signal transduction. Beyond its canonical role in ATP synthesis, NAD serves as an obligate cofactor for enzymes including poly(ADP-ribose) polymerases (PARPs), sirtuins, and CD38, thereby regulating DNA repair, epigenetic remodeling, and inflammatory signaling. Thus, NAD metabolism supports the preservation of cellular homeostasis against oncogenic insults. Malignant transformation, however, imposes substantial biosynthetic and genotoxic stress, often driving metabolic adaptations that amplify NAD production via nicotinamide phosphoribosyltransferase (NAMPT). This endows cancer cells with enhanced proliferative capacity, stress tolerance, and immunoevasive features. Importantly, the dependence of malignant cells on sustained NAD availability constitutes a therapeutically exploitable vulnerability. Accordingly, NAMPT inhibitors, PARP inhibitors, and strategies targeting NAD-consuming ectoenzymes have shown preclinical and, in select settings, clinical efficacy. Here, we critically review the rewiring of NAD metabolism in cancer, associated therapeutic opportunities, and barriers to their clinical exploitation.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"19 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149173067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An NAD+-responsive adipose signal coordinates inter-organ defense against muscle atrophy NAD+反应性脂肪信号协调器官间防御肌肉萎缩

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-14 DOI: 10.1016/j.cmet.2026.09.016

Na Liang,Jia He,Xiangji Guo,Jiaqi Yan,Xiaoqian Zhang,Xiaozhong Peng,Jun Li

引用次数: 0

TNF compromises intestinal bile-acid tolerance dictating colitis progression and limited infliximab response TNF损害肠胆汁酸耐受性，决定结肠炎的进展和有限的英夫利昔单抗反应

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-13 DOI: 10.1016/j.cmet.2026.10.007

Mengqi Zheng,Yunjiao Zhai,Yanbo Yu,Jing Shen,Shuzheng Chu,Enrico Focaccia,Wenyu Tian,Sui Wang,Xuesong Liu,Xi Yuan,Yue Wang,Lixiang Li,Bingcheng Feng,Zhen Li,Xiaohuan Guo,Ju Qiu,Cuijuan Zhang,Jiajie Hou,Yiyuan Sun,Xiaoyun Yang,Xiuli Zuo,Mathias Heikenwalder,Yanqing Li,Detian Yuan,Shiyang Li

引用次数: 0

Cancer-cell-derived fumarate suppresses the anti-tumor capacity of CD8+ T cells in the tumor microenvironment 癌细胞来源的富马酸抑制肿瘤微环境中CD8+ T细胞的抗肿瘤能力

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-13 DOI: 10.1016/j.cmet.2026.10.006

Jie Cheng,Jinxin Yan,Ying Liu,Jiangzhou Shi,Haoyu Wang,Hanyang Zhou,Yinglin Zhou,Tongcun Zhang,Lina Zhao,Xianbin Meng,Haipeng Gong,Xinxiang Zhang,Haichuan Zhu,Peng Jiang

引用次数: 0

Histone lactylation scarring transmits metabolic and epigenetic memory across the gut-liver axis 组蛋白乳酸化疤痕通过肠-肝轴传递代谢和表观遗传记忆

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-07 DOI: 10.1016/j.cmet.2026.09.008

Heng Dong,Jinyang Li,Daowei Yang,Sheng Zhou,Abhinav Choubey,Tiantian Wang,Ruobing Du,Shiyan Li,Huilian Shi,Xiaolei Zhu,Rong Wang

{"title":"Histone lactylation scarring transmits metabolic and epigenetic memory across the gut-liver axis","authors":"Heng Dong,Jinyang Li,Daowei Yang,Sheng Zhou,Abhinav Choubey,Tiantian Wang,Ruobing Du,Shiyan Li,Huilian Shi,Xiaolei Zhu,Rong Wang","doi":"10.1016/j.cmet.2026.09.008","DOIUrl":"https://doi.org/10.1016/j.cmet.2026.09.008","url":null,"abstract":"Ulcerative colitis (UC) remission does not abolish susceptibility to metabolic dysfunction-associated steatotic liver disease (MASLD), but the mechanism linking prior intestinal inflammation to delayed liver injury remains unclear. We establish gut-liver axis memory transduction as an epigenetic-cellular-organ cascade in which inflammatory history is molecularly encoded and redeployed across organs. LCN2+ colonic macrophages persist after colitis resolution and retain heightened glycolysis together with durable histone H3K9 L-lactylation (H3K9la). These macrophages maintain a permissive memory state during remission and traffic to the liver, where they amplify steatosis under subsequent HFD challenge. Mechanistically, BRG1 cooperates with CEBPB at H3K9la-marked chromatin to sustain Lcn2 and Pkm transcription in a feed-forward circuit. Myeloid-specific Smarca4 deletion or pharmacological interruption of macrophage trafficking attenuates macrophage memory and protects against MASLD. Together, our findings define H3K9la-centered macrophage memory as a mobile pathogenic imprint that links prior colitis to increased susceptibility to metabolic liver disease.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"19 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149090102","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Trajectories in immunometabolism 免疫代谢的轨迹

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-06 DOI: 10.1016/j.cmet.2026.09.009

Dirk Brenner,Michela Matteoli,Carole L. Linster,Felix M. Wensveen,Thekla Cordes,Rafael J. Argüello,Claudia Mauri,Christoph Wilhelm,Stefanie K. Wculek,Luke O’Neill,Mari-Carmen Fernández-Agüera

引用次数: 0

Diet-microbiome interactions enhance cancer immunotherapy in obesity 饮食-微生物组的相互作用增强了肥胖患者的癌症免疫治疗

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-06 DOI: 10.1016/j.cmet.2026.08.021

Allard W.J. van Renterghem,Emile E. Voest

引用次数: 0

Pyroptosis, not necroptosis, drives lipid-induced CD4+ T cell death 焦亡，而不是坏死，驱动脂质诱导的CD4+ T细胞死亡

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-06 DOI: 10.1016/j.cmet.2026.08.004

Cornelia M. Weyand,Murari N. Kothagundla,Jose Morales,Lina E. Werner,Brandon Wong,Jörg J. Goronzy

引用次数: 0