{"title":"Stress triggers irritable bowel syndrome with diarrhea through a spermidine-mediated decline in type I interferon","authors":"Li Zhang, Hao-li Wang, Ya-fang Zhang, Xin-tao Mao, Ting-ting Wu, Zhi-hui Huang, Wan-jun Jiang, Ke-qi Fan, Dan-dan Liu, Bing Yang, Mei-hui Zhuang, Guang-ming Huang, Yinming Liang, Shu Jeffrey Zhu, Jiang-yan Zhong, Guang-yin Xu, Xiao-ming Li, Qian Cao, Yi-yuan Li, Jin Jin","doi":"10.1016/j.cmet.2024.09.002","DOIUrl":"https://doi.org/10.1016/j.cmet.2024.09.002","url":null,"abstract":"Irritable bowel syndrome with diarrhea (IBS-D) is a common and chronic gastrointestinal disorder that is characterized by abdominal discomfort and occasional diarrhea. The pathogenesis of IBS-D is thought to be related to a combination of factors, including psychological stress, abnormal muscle contractions, and inflammation and disorder of the gut microbiome. However, there is still a lack of comprehensive analysis of the logical regulatory correlation among these factors. In this study, we found that stress induced hyperproduction of xanthine and altered the abundance and metabolic characteristics of <em>Lactobacillus murinus</em> in the gut. <em>Lactobacillus murinus</em>-derived spermidine suppressed the basal expression of type I interferon (IFN)-α in plasmacytoid dendritic cells by inhibiting the K63-linked polyubiquitination of TRAF3. The reduction in IFN-α unrestricted the contractile function of colonic smooth muscle cells, resulting in an increase in bowel movement. Our findings provided a theoretical basis for the pathological mechanism of, and new drug targets for, stress-exposed IBS-D.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"7 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142369148","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}
Cell metabolismPub Date : 2024-10-01DOI: 10.1016/j.cmet.2024.09.005
Tuo Shao, Raymond T. Chung
{"title":"Ironing out MAFLD: Therapeutic targeting of liver ferroptosis","authors":"Tuo Shao, Raymond T. Chung","doi":"10.1016/j.cmet.2024.09.005","DOIUrl":"https://doi.org/10.1016/j.cmet.2024.09.005","url":null,"abstract":"Metabolic dysfunction-associated fatty liver disease (MAFLD) is associated with iron metabolism disorders and ferroptosis, but the mechanisms underlying this association remain unclear. Fudi Wang’s group<span><span><sup>1</sup></span></span> used animal models, human cohorts, and multi-omics data to demonstrate the role of iron imbalance in MAFLD and the therapeutic potential of the iron chelator FerroTerminator 1 (FOT1).","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"25 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142360545","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}
Cell metabolismPub Date : 2024-10-01DOI: 10.1016/j.cmet.2024.09.001
Jessica D. Ewald, Yao Lu, Cara E. Ellis, Jessica Worton, Jelena Kolic, Shugo Sasaki, Dahai Zhang, Theodore dos Santos, Aliya F. Spigelman, Austin Bautista, Xiao-Qing Dai, James G. Lyon, Nancy P. Smith, Jordan M. Wong, Varsha Rajesh, Han Sun, Seth A. Sharp, Jason C. Rogalski, Renata Moravcova, Haoning H. Cen, Patrick E. MacDonald
{"title":"HumanIslets.com: Improving accessibility, integration, and usability of human research islet data","authors":"Jessica D. Ewald, Yao Lu, Cara E. Ellis, Jessica Worton, Jelena Kolic, Shugo Sasaki, Dahai Zhang, Theodore dos Santos, Aliya F. Spigelman, Austin Bautista, Xiao-Qing Dai, James G. Lyon, Nancy P. Smith, Jordan M. Wong, Varsha Rajesh, Han Sun, Seth A. Sharp, Jason C. Rogalski, Renata Moravcova, Haoning H. Cen, Patrick E. MacDonald","doi":"10.1016/j.cmet.2024.09.001","DOIUrl":"https://doi.org/10.1016/j.cmet.2024.09.001","url":null,"abstract":"HumanIslets.com supports diabetes research by offering easy access to islet phenotyping data, analysis tools, and data download. It includes molecular omics, islet and cellular function assays, tissue processing metadata, and phenotypes from 547 donors. As it expands, the resource aims to improve human islet data quality, usability, and accessibility.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"111 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142360161","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}
Cell metabolismPub Date : 2024-10-01DOI: 10.1016/j.cmet.2024.09.003
Bandy Chen, Xiaofei Yu, Claudia Horvath-Diano, María José Ortuño, Matthias H. Tschöp, Ania M. Jastreboff, Marc Schneeberger
{"title":"GLP-1 programs the neurovascular landscape","authors":"Bandy Chen, Xiaofei Yu, Claudia Horvath-Diano, María José Ortuño, Matthias H. Tschöp, Ania M. Jastreboff, Marc Schneeberger","doi":"10.1016/j.cmet.2024.09.003","DOIUrl":"https://doi.org/10.1016/j.cmet.2024.09.003","url":null,"abstract":"Readily available nutrient-rich foods exploit our inherent drive to overconsume, creating an environment of overnutrition. This transformative setting has led to persistent health issues, such as obesity and metabolic syndrome. The development of glucagon-like peptide-1 receptor (GLP-1R) agonists reveals our ability to pharmacologically manage weight and address metabolic conditions. Obesity is directly linked to chronic low-grade inflammation, connecting our metabolic environment to neurodegenerative diseases. GLP-1R agonism in curbing obesity, achieved by impacting appetite and addressing associated metabolic defects, is revealing additional benefits extending beyond weight loss. Whether GLP-1R agonism directly impacts brain health or does so indirectly through improved metabolic health remains to be elucidated. In exploring the intricate connection between obesity and neurological conditions, recent literature suggests that GLP-1R agonism may have the capacity to shape the neurovascular landscape. Thus, GLP-1R agonism emerges as a promising strategy for addressing the complex interplay between metabolic health and cognitive well-being.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"8 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142360186","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}
Cell metabolismPub Date : 2024-10-01DOI: 10.1016/j.cmet.2024.09.004
Miguel López
{"title":"Cortical actions of thyroid hormone: An exploration and metabolism crossroad","authors":"Miguel López","doi":"10.1016/j.cmet.2024.09.004","DOIUrl":"https://doi.org/10.1016/j.cmet.2024.09.004","url":null,"abstract":"Classically, the central actions of thyroid hormones (THs) on metabolism occur within the hypothalamus. A recent article published in <em>Cell</em> by Sabatini and colleagues demonstrates that TH modulates cerebral cortical circuits of male mice, which might integrate exploratory behavior and whole-body metabolism.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"66 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142360185","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}
Cell metabolismPub Date : 2024-09-23DOI: 10.1016/j.cmet.2024.08.012
Peng Zhang, Junlai Liu, Allen Lee, Irene Tsaur, Masafumi Ohira, Vivian Duong, Nicholas Vo, Kosuke Watari, Hua Su, Ju Youn Kim, Li Gu, Mandy Zhu, Shabnam Shalapour, Mojgan Hosseini, Gautam Bandyopadhyay, Suling Zeng, Cristina Llorente, Haoqi Nina Zhao, Santosh Lamichhane, Siddharth Mohan, Michael Karin
{"title":"IL-22 resolves MASLD via enterocyte STAT3 restoration of diet-perturbed intestinal homeostasis","authors":"Peng Zhang, Junlai Liu, Allen Lee, Irene Tsaur, Masafumi Ohira, Vivian Duong, Nicholas Vo, Kosuke Watari, Hua Su, Ju Youn Kim, Li Gu, Mandy Zhu, Shabnam Shalapour, Mojgan Hosseini, Gautam Bandyopadhyay, Suling Zeng, Cristina Llorente, Haoqi Nina Zhao, Santosh Lamichhane, Siddharth Mohan, Michael Karin","doi":"10.1016/j.cmet.2024.08.012","DOIUrl":"https://doi.org/10.1016/j.cmet.2024.08.012","url":null,"abstract":"The exponential rise in metabolic dysfunction-associated steatotic liver disease (MASLD) parallels the ever-increasing consumption of energy-dense diets, underscoring the need for effective MASLD-resolving drugs. MASLD pathogenesis is linked to obesity, diabetes, “gut-liver axis” alterations, and defective interleukin-22 (IL-22) signaling. Although barrier-protective IL-22 blunts diet-induced metabolic alterations, inhibits lipid intake, and reverses microbial dysbiosis, obesogenic diets rapidly suppress its production by small intestine-localized innate lymphocytes. This results in STAT3 inhibition in intestinal epithelial cells (IECs) and expansion of the absorptive enterocyte compartment. These MASLD-sustaining aberrations were reversed by administration of recombinant IL-22, which resolved hepatosteatosis, inflammation, fibrosis, and insulin resistance. Exogenous IL-22 exerted its therapeutic effects through its IEC receptor, rather than hepatocytes, activating STAT3 and inhibiting WNT-β-catenin signaling to shrink the absorptive enterocyte compartment. By reversing diet-reinforced macronutrient absorption, the main source of liver lipids, IL-22 signaling restoration represents a potentially effective interception of dietary obesity and MASLD.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"21 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142276831","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}
Cell metabolismPub Date : 2024-09-20DOI: 10.1016/j.cmet.2024.08.010
Xiaoli Wei, Dongqing Wu, Jing Li, Miaomiao Wu, Qianhui Li, Zhaodi Che, Xu Cheng, Qianying Cheng, Fan Yin, Hao Zhang, Xuefu Wang, Shabnam Abtahi, Li Zuo, Lei Hang, Lili Ma, Wei-Ting Kuo, Xiaoying Liu, Jerrold R. Turner, Hua Wang, Jia Xiao, Fei Wang
{"title":"Myeloid beta-arrestin 2 depletion attenuates metabolic dysfunction-associated steatohepatitis via the metabolic reprogramming of macrophages","authors":"Xiaoli Wei, Dongqing Wu, Jing Li, Miaomiao Wu, Qianhui Li, Zhaodi Che, Xu Cheng, Qianying Cheng, Fan Yin, Hao Zhang, Xuefu Wang, Shabnam Abtahi, Li Zuo, Lei Hang, Lili Ma, Wei-Ting Kuo, Xiaoying Liu, Jerrold R. Turner, Hua Wang, Jia Xiao, Fei Wang","doi":"10.1016/j.cmet.2024.08.010","DOIUrl":"https://doi.org/10.1016/j.cmet.2024.08.010","url":null,"abstract":"<p>Macrophage-mediated inflammation has been implicated in the pathogenesis of metabolic dysfunction-associated steatohepatitis (MASH); however, the immunometabolic program underlying the regulation of macrophage activation remains unclear. Beta-arrestin 2, a multifunctional adaptor protein, is highly expressed in bone marrow tissues and macrophages and is involved in metabolism disorders. Here, we observed that β-arrestin 2 expression was significantly increased in the liver macrophages and circulating monocytes of patients with MASH compared with healthy controls and positively correlated with the severity of metabolic dysfunction-associated steatotic liver disease (MASLD). Global or myeloid <em>Arrb2</em> deficiency prevented the development of MASH in mice. Further study showed that β-arrestin 2 acted as an adaptor protein and promoted ubiquitination of immune responsive gene 1 (IRG1) to prevent increased itaconate production in macrophages, which resulted in enhanced succinate dehydrogenase activity, thereby promoting the release of mitochondrial reactive oxygen species and M1 polarization. Myeloid β-arrestin 2 depletion may be a potential approach for MASH.</p>","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"114 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142273520","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}
Cell metabolismPub Date : 2024-09-17DOI: 10.1016/j.cmet.2024.08.009
Jia-Hui Luo, Fa-Xi Wang, Jia-Wei Zhao, Chun-Liang Yang, Shan-Jie Rong, Wan-Ying Lu, Qi-Jie Chen, Qing Zhou, Jun Xiao, Ya-Nan Wang, Xi Luo, Yang Li, Dan-Ni Song, Cai Chen, Cheng-Liang Zhang, Su-Hua Chen, Ping Yang, Fei Xiong, Qi-Lin Yu, Shu Zhang, Cong-Yi Wang
{"title":"PDIA3 defines a novel subset of adipose macrophages to exacerbate the development of obesity and metabolic disorders","authors":"Jia-Hui Luo, Fa-Xi Wang, Jia-Wei Zhao, Chun-Liang Yang, Shan-Jie Rong, Wan-Ying Lu, Qi-Jie Chen, Qing Zhou, Jun Xiao, Ya-Nan Wang, Xi Luo, Yang Li, Dan-Ni Song, Cai Chen, Cheng-Liang Zhang, Su-Hua Chen, Ping Yang, Fei Xiong, Qi-Lin Yu, Shu Zhang, Cong-Yi Wang","doi":"10.1016/j.cmet.2024.08.009","DOIUrl":"https://doi.org/10.1016/j.cmet.2024.08.009","url":null,"abstract":"<p>Adipose tissue macrophages (ATMs) play important roles in maintaining adipose tissue homeostasis and orchestrating metabolic inflammation. Given the extensive functional heterogeneity and phenotypic plasticity of ATMs, identification of the authentically pathogenic ATM subpopulation under obese setting is thus necessitated. Herein, we performed single-nucleus RNA sequencing (snRNA-seq) and unraveled a unique maladaptive ATM subpopulation defined as ATF4<sup>hi</sup>PDIA3<sup>hi</sup>ACSL4<sup>hi</sup>CCL2<sup>hi</sup> inflammatory and metabolically activated macrophages (iMAMs), in which PDIA3 is required for the maintenance of their migratory and pro-inflammatory properties. Mechanistically, ATF4 serves as a metabolic stress sensor to transcribe PDIA3, which then imposes a redox control on RhoA activity and strengthens the pro-inflammatory and migratory properties of iMAMs through RhoA-YAP signaling. Administration of <em>Pdia3</em> small interfering RNA (siRNA)-loaded liposomes effectively repressed adipose inflammation and high-fat diet (HFD)-induced obesity. Together, our data support that strategies aimed at targeting iMAMs by suppressing PDIA3 expression or activity could be a viable approach against obesity and metabolic disorders in clinical settings.</p>","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"13 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142235502","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}
Cell metabolismPub Date : 2024-09-12DOI: 10.1016/j.cmet.2024.08.008
Jing Zhang, Kim Anker Sjøberg, Songlin Gong, Tongtong Wang, Fengqi Li, Andrew Kuo, Stephan Durot, Adam Majcher, Raphaela Ardicoglu, Thibaut Desgeorges, Charlotte Greta Mann, Ines Soro Arnáiz, Gillian Fitzgerald, Paola Gilardoni, E. Dale Abel, Shigeyuki Kon, Danyvid Olivares-Villagómez, Nicola Zamboni, Christian Wolfrum, Thorsten Hornemann, Katrien De Bock
{"title":"Endothelial metabolic control of insulin sensitivity through resident macrophages","authors":"Jing Zhang, Kim Anker Sjøberg, Songlin Gong, Tongtong Wang, Fengqi Li, Andrew Kuo, Stephan Durot, Adam Majcher, Raphaela Ardicoglu, Thibaut Desgeorges, Charlotte Greta Mann, Ines Soro Arnáiz, Gillian Fitzgerald, Paola Gilardoni, E. Dale Abel, Shigeyuki Kon, Danyvid Olivares-Villagómez, Nicola Zamboni, Christian Wolfrum, Thorsten Hornemann, Katrien De Bock","doi":"10.1016/j.cmet.2024.08.008","DOIUrl":"https://doi.org/10.1016/j.cmet.2024.08.008","url":null,"abstract":"<p>Endothelial cells (ECs) not only form passive blood conduits but actively contribute to nutrient transport and organ homeostasis. The role of ECs in glucose homeostasis is, however, poorly understood. Here, we show that, in skeletal muscle, endothelial glucose transporter 1 (<em>Glut1</em>/Slc2a1) controls glucose uptake via vascular metabolic control of muscle-resident macrophages <em>without</em> affecting transendothelial glucose transport. Lowering endothelial <em>Glut1</em> via genetic depletion (<em>Glut1</em><sup>ΔEC</sup>) or upon a short-term high-fat diet increased angiocrine osteopontin (OPN/<em>Spp1</em>) secretion. This promoted resident muscle macrophage activation and proliferation, which impaired muscle insulin sensitivity. Consequently, co-deleting <em>Spp1</em> from ECs prevented macrophage accumulation and improved insulin sensitivity in <em>Glut1</em><sup>ΔEC</sup> mice. Mechanistically, <em>Glut1-</em>dependent endothelial glucose metabolic rewiring increased OPN in a serine metabolism-dependent fashion. Our data illustrate how the glycolytic endothelium creates a microenvironment that controls resident muscle macrophage phenotype and function and directly links resident muscle macrophages to the maintenance of muscle glucose homeostasis.</p>","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"22 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142171420","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}
Cell metabolismPub Date : 2024-09-10DOI: 10.1016/j.cmet.2024.08.007
Fopei Ma, Zhuang Li, Haihua Liu, Shixian Chen, Songyuan Zheng, Junqing Zhu, Hao Shi, Haixin Ye, Zhantu Qiu, Lei Gao, Bingqi Han, Qian Yang, Xing Wang, Yang Zhang, Lifang Cheng, Huijie Fan, Shuaijun Lv, Xiaoshan Zhao, Hongwei Zhou, Juan Li, Mukeng Hong
{"title":"Dietary-timing-induced gut microbiota diurnal oscillations modulate inflammatory rhythms in rheumatoid arthritis","authors":"Fopei Ma, Zhuang Li, Haihua Liu, Shixian Chen, Songyuan Zheng, Junqing Zhu, Hao Shi, Haixin Ye, Zhantu Qiu, Lei Gao, Bingqi Han, Qian Yang, Xing Wang, Yang Zhang, Lifang Cheng, Huijie Fan, Shuaijun Lv, Xiaoshan Zhao, Hongwei Zhou, Juan Li, Mukeng Hong","doi":"10.1016/j.cmet.2024.08.007","DOIUrl":"https://doi.org/10.1016/j.cmet.2024.08.007","url":null,"abstract":"<p>Rheumatoid arthritis (RA) is a chronic autoimmune condition characterized by inflammatory activity with distinct rhythmic fluctuations. However, the precise mechanisms governing these inflammatory rhythms remain elusive. Here, we explore the interaction between dietary patterns, gut microbiota diurnal oscillations, and the rhythmicity of RA in both collagen-induced arthritis (CIA) mice and patients with RA and highlight the significance of dietary timing in modulating RA inflammatory rhythms linked to gut microbiota. Specifically, we discovered that <em>Parabacteroides distasonis</em> (<em>P. distasonis</em>) uses β-glucosidase (β-GC) to release glycitein (GLY) from the diet in response to daily nutritional cues, influencing RA inflammatory rhythms dependent on the sirtuin 5-nuclear factor-κB (SIRT5-NF-κB) axis. Notably, we validated the daily fluctuations of <em>P. distasonis-</em>β-GC-GLY in patients with RA through continuous sampling across day-night cycles. These findings underscore the crucial role of dietary timing in RA rhythmicity and propose potential clinical implications for novel therapeutic strategies to alleviate arthritis.</p>","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"1 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142160996","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}
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