Cell metabolism最新文献_第2页

Metabolic advantages of a high-protein, low-carbohydrate diet in in patients with metabolically unhealthy obesity 高蛋白、低碳水化合物饮食在代谢不健康肥胖患者中的代谢优势

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-06 DOI: 10.1016/j.cmet.2026.08.016

Nicola Guess

引用次数: 0

Glutamine metabolism keeps pathogenic hepatic CD4+ T cells in check 谷氨酰胺代谢使致病性肝CD4+ T细胞受到控制

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-06 DOI: 10.1016/j.cmet.2026.09.004

Haiguang Wang,Andrew Hakeem,Xavier S. Revelo

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Oleic acid might induce necroptosis of CD4+ T cells, in addition to its induction of pyroptosis 油酸除诱导凋亡外，还可诱导CD4+ T细胞坏死

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-06 DOI: 10.1016/j.cmet.2026.07.021

Caglar Berkel

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You are what you eat and translate: Feeding the code to fight cancer and viruses 你吃什么就是什么，并翻译为：提供对抗癌症和病毒的代码

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-06 DOI: 10.1016/j.cmet.2026.09.006

Adrianna Dabrowska,Davide Ruggero

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Fungus Rhizopus arrhizus promotes MASLD-associated hepatocellular carcinoma through generating kynurenic acid 真菌阿根霉通过产生乳酸促进masld相关的肝细胞癌

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-01 DOI: 10.1016/j.cmet.2026.09.005

Xingyu Zhou,Chuanfa Liu,Wenchao Wei,Xueliang Wang,Yasi Pan,Ying Jiao,Shiyu Li,Yating Zhang,Harry Cheuk-Hay Lau,Ruyi Zhang,Dingwu Li,Alvin Ho-Kwan Cheung,Minghua Zheng,Wen Pan,Chi Chun Wong,Vincent Wai-Sun Wong,Jun Yu,Xiang Zhang

引用次数: 0

Lipid droplet-induced T cell death sustains autoimmune tissue inflammation 脂滴诱导的T细胞死亡维持自身免疫组织炎症

IF 29 1区生物学

Cell metabolism Pub Date : 2026-10-01 DOI: 10.1016/j.cmet.2026.10.003

Jitendra Kumar,Yoshinori Takashima,Jose Morales,Brandon Wong,Lina Werner,Isabel N. Goronzy,Selene Rubino,Robert T. Trousdale,Gerald J. Berry,Jörg J. Goronzy,Cornelia M. Weyand

引用次数: 0

Microbial aldehyde-alcohol dehydrogenase degrades metformin to limit therapeutic response in type 2 diabetes 微生物醛醇脱氢酶降解二甲双胍以限制2型糖尿病的治疗反应

IF 29 1区生物学

Cell metabolism Pub Date : 2026-09-29 DOI: 10.1016/j.cmet.2026.09.003

Yue Zhao,Chen Peng,Ying Xia,Tiejun Dong,Juan Xu,Xiaodong Shan,Xiang Zhong,Jingchuan Xue,Ziqian Bing,Pengfei Li,Jingyu Han,Yunzhong Nie,Kelei He,Yu Cao,Tingting Wang

{"title":"Microbial aldehyde-alcohol dehydrogenase degrades metformin to limit therapeutic response in type 2 diabetes","authors":"Yue Zhao,Chen Peng,Ying Xia,Tiejun Dong,Juan Xu,Xiaodong Shan,Xiang Zhong,Jingchuan Xue,Ziqian Bing,Pengfei Li,Jingyu Han,Yunzhong Nie,Kelei He,Yu Cao,Tingting Wang","doi":"10.1016/j.cmet.2026.09.003","DOIUrl":"https://doi.org/10.1016/j.cmet.2026.09.003","url":null,"abstract":"Metformin is a first-line therapy for type 2 diabetes, yet therapeutic responses vary widely. Whether gut microbes directly inactivate metformin and limit its efficacy remains unclear. Here, we identify a gut microbial aldehyde-alcohol dehydrogenase, AdhE, from Eubacterium species enriched in individuals with a low response to metformin. AdhE converts metformin to pharmacologically inactive products, lowering intestinal and systemic drug exposure. Genetic deletion of AdhE or phage-mediated depletion of AdhE-producing Eubacterium hallii MD1 restores metformin exposure and glycemic control in mice. An artificial intelligence-guided structure-based screen identifies the dietary phytochemical daidzein as a microbial AdhE inhibitor that blocks metformin degradation and improves metformin responsiveness. These findings establish gut microbial drug inactivation as a modifiable determinant of therapeutic response and provide a framework for microbial enzyme-guided strategies to improve established therapies.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"33 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149070994","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

Adipose ILC2s depend on acetyl-CoA carboxylase 1 to maintain metabolic health 脂肪ILC2s依赖于乙酰辅酶a羧化酶1来维持代谢健康

IF 29 1区生物学

Cell metabolism Pub Date : 2026-09-23 DOI: 10.1016/j.cmet.2026.08.019

Fotios Karagiannis,Maria Rafailia Theodorou,Fabian Nikolka,Maria Doverman,Dhruvi Shah,Chantal Wientjens,Timothy R. McCulloch,Ronja Kardinal,David Colon,Jelena Zurkovic,Jiangyan Yu,Julia Anna Noras,Patricia Weiss,Roman Rombo,Tim Sparwasser,Zeinab Abdullah,Felix Meissner,Christoph Thiele,Jan Hasenauer,Dagmar Wachten,Karsten Hiller,Christoph Wilhelm

{"title":"Adipose ILC2s depend on acetyl-CoA carboxylase 1 to maintain metabolic health","authors":"Fotios Karagiannis,Maria Rafailia Theodorou,Fabian Nikolka,Maria Doverman,Dhruvi Shah,Chantal Wientjens,Timothy R. McCulloch,Ronja Kardinal,David Colon,Jelena Zurkovic,Jiangyan Yu,Julia Anna Noras,Patricia Weiss,Roman Rombo,Tim Sparwasser,Zeinab Abdullah,Felix Meissner,Christoph Thiele,Jan Hasenauer,Dagmar Wachten,Karsten Hiller,Christoph Wilhelm","doi":"10.1016/j.cmet.2026.08.019","DOIUrl":"https://doi.org/10.1016/j.cmet.2026.08.019","url":null,"abstract":"Adipose group 2 innate lymphoid cells (ILC2s) are essential to maintain metabolic homeostasis. Obesity severely impairs the number and function of ILC2s, resulting in the progression of metabolic inflammation. How ILC2s are perturbed in obesity remains unknown. Here, we find that high-fat diet (HFD)-induced obesity in mice increases fatty acid oxidation, leading to suppression of acetyl-coenzyme A (CoA) carboxylase 1 (ACC1) in adipose ILC2s. ACC1 is essential for maintaining the citrate shuttle, NAD+/NADH balance, and cellular metabolism. Mimicking the effects of HFD, ACC1 deletion impairs differentiation, maintenance, and function of ILC2s. This results in adipose tissue hypertrophy and inflammation at steady state, predisposing mice to the development of diabetes. Supplementing with the NAD+ precursor nicotinamide riboside rescues ACC1 deficiency, restoring ILC2 function and adipose tissue homeostasis. These findings establish ACC1 as a critical regulator of adipose ILC2 maintenance and function and provide a rationale for the adverse effects of ACC inhibition in obesity.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"76 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149019673","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

Lactate couples metabolic state to necroptosis across pathological and physiological conditions 乳酸通过病理和生理条件将代谢状态与坏死性下垂联系起来

IF 29 1区生物学

Cell metabolism Pub Date : 2026-09-23 DOI: 10.1016/j.cmet.2026.08.022

Naijin Zhang,Xinyue Huang,Saien Lu,Yuanming Zou,Guozhe Sun,Wei Zhang,Huijun Lu,Limin Wang,Xinxin Lu,Zhaobo Zhang,Cheng Cheng,Shilong You,He Zhang,Ying Zhang,Pengbo Wang,Pan Zhou,Juan Luo,Yuyi Chen,Feng Wu,Jiayan Guo,Anqi Ning,Yushan Guo,Liu Cao,Liming Sun,Yingxian Sun

{"title":"Lactate couples metabolic state to necroptosis across pathological and physiological conditions","authors":"Naijin Zhang,Xinyue Huang,Saien Lu,Yuanming Zou,Guozhe Sun,Wei Zhang,Huijun Lu,Limin Wang,Xinxin Lu,Zhaobo Zhang,Cheng Cheng,Shilong You,He Zhang,Ying Zhang,Pengbo Wang,Pan Zhou,Juan Luo,Yuyi Chen,Feng Wu,Jiayan Guo,Anqi Ning,Yushan Guo,Liu Cao,Liming Sun,Yingxian Sun","doi":"10.1016/j.cmet.2026.08.022","DOIUrl":"https://doi.org/10.1016/j.cmet.2026.08.022","url":null,"abstract":"How fluctuations in central metabolites are transduced into cell-death decisions remains poorly understood. Here we show that lactate directly promotes necroptosis through lactylation of receptor-interacting protein kinase 3 (RIPK3) at lysine 63 (K63). Large-scale screening identified LDH inhibition as a suppressor of mixed lineage kinase domain-like pseudokinase (MLKL)-dependent necroptosis, implicating intracellular lactate as a pivotal modulator. PCAF-mediated K63 lactylation enhances RIPK3 kinase activity and stabilizes the RIPK3-MLKL complex, driving membrane disruption. K63R mutation or PCAF loss potently suppresses necroptosis. This pathway operates in both pathological and physiological contexts: K63R knockin mice and LDH/PCAF inhibition protect against injury in myocardial ischemia-reperfusion and influenza A infection, whereas exercise-induced lactate engages the identical cascade to drive myofiber necroptosis, activating muscle stem cells and enhancing athletic performance. These findings reveal RIPK3-K63 lactylation as a pivotal mechanism linking lactate fluctuations to cell-death outcomes across disease and physiology.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"18 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149019668","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

Adipocytes: Hidden forces of the immune system? 脂肪细胞：免疫系统的隐藏力量？

IF 29 1区生物学

Cell metabolism Pub Date : 2026-09-23 DOI: 10.1016/j.cmet.2026.08.020

Julia Zinngrebe,Konstantin M.J. Sparrer,Pamela Fischer-Posovszky

引用次数: 0