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“Shunt-ing” down obesity with novel endogenous metabolites 用新的内源性代谢物“分流”肥胖
IF 29 1区 生物学
Cell metabolism Pub Date : 2025-03-04 DOI: 10.1016/j.cmet.2025.02.005
Victor J. Pai, Alan Saghatelian
{"title":"“Shunt-ing” down obesity with novel endogenous metabolites","authors":"Victor J. Pai, Alan Saghatelian","doi":"10.1016/j.cmet.2025.02.005","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.02.005","url":null,"abstract":"Obesity is a growing public health issue that has recently been transformed through the advent of new medicines. However, our understanding of the pathways and mechanisms that regulate energy balance in mammals is still developing. Recent discoveries on this front include an exciting new finding that there exists a novel class of metabolites in humans and mice that can regulate obesity in rodents.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"190 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539038","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 cellular and molecular basis of leptin resistance 瘦素抵抗的细胞和分子基础
IF 29 1区 生物学
Cell metabolism Pub Date : 2025-03-04 DOI: 10.1016/j.cmet.2025.01.001
Bowen Tan, Kristina Hedbacker, Leah Kelly, Zhaoyue Zhang, Alexandre Moura-Assis, Ji-Dung Luo, Joshua D. Rabinowitz, Jeffrey M. Friedman
{"title":"A cellular and molecular basis of leptin resistance","authors":"Bowen Tan, Kristina Hedbacker, Leah Kelly, Zhaoyue Zhang, Alexandre Moura-Assis, Ji-Dung Luo, Joshua D. Rabinowitz, Jeffrey M. Friedman","doi":"10.1016/j.cmet.2025.01.001","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.01.001","url":null,"abstract":"Similar to most humans with obesity, diet-induced obese (DIO) mice have high leptin levels and fail to respond to the exogenous hormone, suggesting that their obesity is caused by leptin resistance, the pathogenesis of which is unknown. We found that leptin treatment reduced plasma levels of leucine and methionine, mTOR-activating ligands, leading us to hypothesize that chronic mTOR activation might reduce leptin signaling. Rapamycin, an mTOR inhibitor, reduced fat mass and increased leptin sensitivity in DIO mice but not in mice with defects in leptin signaling. Rapamycin restored leptin’s actions on POMC neurons and failed to reduce the weight of mice with defects in melanocortin signaling. mTOR activation in POMC neurons caused leptin resistance, whereas POMC-specific mutations in mTOR activators decreased weight gain of DIO mice. Thus, increased mTOR activity in POMC neurons is necessary and sufficient for the development of leptin resistance in DIO mice, establishing a key pathogenic mechanism leading to obesity.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"6 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539122","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
Brain dopamine responses to ultra-processed milkshakes are highly variable and not significantly related to adiposity in humans 脑多巴胺对超加工奶昔的反应是高度可变的，与人类肥胖没有显著关系
IF 29 1区 生物学
Cell metabolism Pub Date : 2025-03-04 DOI: 10.1016/j.cmet.2025.02.002
Valerie L. Darcey, Juen Guo, Meible Chi, Stephanie T. Chung, Amber B. Courville, Isabelle Gallagher, Peter Herscovitch, Paule V. Joseph, Rebecca Howard, Melissa La Noire, Lauren Milley, Alex Schick, Michael Stagliano, Sara Turner, Nicholas Urbanski, Shanna Yang, Nan Zhai, Megan S. Zhou, Kevin D. Hall
{"title":"Brain dopamine responses to ultra-processed milkshakes are highly variable and not significantly related to adiposity in humans","authors":"Valerie L. Darcey, Juen Guo, Meible Chi, Stephanie T. Chung, Amber B. Courville, Isabelle Gallagher, Peter Herscovitch, Paule V. Joseph, Rebecca Howard, Melissa La Noire, Lauren Milley, Alex Schick, Michael Stagliano, Sara Turner, Nicholas Urbanski, Shanna Yang, Nan Zhai, Megan S. Zhou, Kevin D. Hall","doi":"10.1016/j.cmet.2025.02.002","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.02.002","url":null,"abstract":"Ultra-processed foods high in fat and sugar have been theorized to be addictive due to their purported ability to induce an exaggerated post-ingestive brain dopamine response akin to drugs of abuse. Using [<sup>11</sup>C]raclopride positron emission tomography (PET) displacement methods used to measure brain dopamine responses to addictive drugs, we measured striatal dopamine responses beginning 30 min after ingesting an ultra-processed milkshake high in fat and sugar in 50 young, healthy adults over a wide body mass index (BMI) range (20–45 kg/m<sup>2</sup>). Surprisingly, milkshake consumption did not result in a significant post-ingestive dopamine response in the striatum (<em>p</em> = 0.62) nor in any striatal subregion (<em>p</em> &gt; 0.33), and the highly variable interindividual responses were not significantly related to adiposity (BMI: <em>r</em> = 0.076, <em>p</em> = 0.51; % body fat: <em>r</em> = 0.16, <em>p</em> = 0.28). Thus, post-ingestive striatal dopamine responses to an ultra-processed milkshake were likely substantially smaller than for many addictive drugs and below the limits of detection using standard PET methods.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"23 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539123","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
On the causes of obesity and its treatment: The end of the beginning 关于肥胖症的原因及其治疗：起点的终点
IF 29 1区 生物学
Cell metabolism Pub Date : 2025-03-04 DOI: 10.1016/j.cmet.2025.01.026
Jeffrey M. Friedman
{"title":"On the causes of obesity and its treatment: The end of the beginning","authors":"Jeffrey M. Friedman","doi":"10.1016/j.cmet.2025.01.026","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.01.026","url":null,"abstract":"Over the last 30 years, our understanding of the causes of obesity has been transformed, and new, highly effective medicines for reducing weight have been developed. This remarkable progress marks an end and a beginning. By establishing that obesity is a biologic disorder amenable to scientific inquiry and rational drug development, simplistic notions about its causes and treatment should be laid to rest. The future holds the promise that additional therapeutic approaches for inducing or maintaining weight loss will be developed, and that these treatments will be tailored to different subgroups to potentially address the pathogenic mechanisms.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"41 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539039","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
Decoding the complex systems of obesity 解码肥胖症的复杂系统
IF 29 1区 生物学
Cell metabolism Pub Date : 2025-03-04 DOI: 10.1016/j.cmet.2025.02.001
Allyson Evans
{"title":"Decoding the complex systems of obesity","authors":"Allyson Evans","doi":"10.1016/j.cmet.2025.02.001","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.02.001","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Main text</h2>We present this special focus issue on March 4th, coinciding with <span><span>World Obesity Day 2025</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span>, to show our solidarity with the World Obesity Federation and advocate for increased awareness, prevention, and treatment of obesity. We embrace this year’s World Obesity Day theme, \"Changing Systems,\" which challenges us to broaden our perspective from viewing obesity as solely an individual issue and recognize the wider systemic factors that contribute to the rapidly escalating rates of obesity worldwide.</section></section>","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"35 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539118","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
Famsin and fasting adaptation: A glucagon connection 饥饿素和禁食适应：胰高血糖素的联系
IF 29 1区 生物学
Cell metabolism Pub Date : 2025-03-04 DOI: 10.1016/j.cmet.2025.01.030
Siming Li, Ziyi Meng, Jiandie D. Lin
{"title":"Famsin and fasting adaptation: A glucagon connection","authors":"Siming Li, Ziyi Meng, Jiandie D. Lin","doi":"10.1016/j.cmet.2025.01.030","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.01.030","url":null,"abstract":"Starvation triggers an organismal adaptive response that is orchestrated by endocrine factors. In this issue of <em>Cell Metabolism</em>, Long et al.<span><span><sup>1</sup></span></span> uncover a famsin-glucagon axis that relays gut-derived hormonal cues to systemic glucose homeostasis during fasting.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"41 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539120","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
SnapShot: Brain-targeting anti-obesity medications 快照：针对大脑的抗肥胖药物
IF 29 1区 生物学
Cell metabolism Pub Date : 2025-03-04 DOI: 10.1016/j.cmet.2025.02.006
Jonas Petersen, Valdemar Brimnes Ingemann Johansen, Christoffer Clemmensen
{"title":"SnapShot: Brain-targeting anti-obesity medications","authors":"Jonas Petersen, Valdemar Brimnes Ingemann Johansen, Christoffer Clemmensen","doi":"10.1016/j.cmet.2025.02.006","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.02.006","url":null,"abstract":"Advances in the understanding of homeostatic regulation of body weight and the neurobiology of appetite, combined with innovations in medicinal chemistry, have paved the way for safe and effective weight loss medications. Long-acting GLP-1 receptor agonists have revolutionized obesity treatment, and, together with emerging GLP-1-based multi-agonists and combination therapies, offer significant potential to combat cardiometabolic diseases and a range of other chronic health challenges. To view this SnapShot, open or download the PDF.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"16 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539124","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
Hepatic stellate cells regulate liver fatty acid utilization via plasmalemma vesicle-associated protein 肝星状细胞通过质膜囊泡相关蛋白调节肝脏对脂肪酸的利用
IF 29 1区 生物学
Cell metabolism Pub Date : 2025-03-03 DOI: 10.1016/j.cmet.2025.01.022
Daniel Hansen, Jasmin E.R. Jensen, Christian A.T. Andersen, Peter R. Jakobsgaard, Jesper Havelund, Line Lauritsen, Samuel Mandacaru, Majken Siersbaek, Oliver L. Shackleton, Hiroshi Inoue, Jonathan R. Brewer, Robert F. Schwabe, Blagoy Blagoev, Nils J. Færgeman, Marko Salmi, Kim Ravnskjaer
{"title":"Hepatic stellate cells regulate liver fatty acid utilization via plasmalemma vesicle-associated protein","authors":"Daniel Hansen, Jasmin E.R. Jensen, Christian A.T. Andersen, Peter R. Jakobsgaard, Jesper Havelund, Line Lauritsen, Samuel Mandacaru, Majken Siersbaek, Oliver L. Shackleton, Hiroshi Inoue, Jonathan R. Brewer, Robert F. Schwabe, Blagoy Blagoev, Nils J. Færgeman, Marko Salmi, Kim Ravnskjaer","doi":"10.1016/j.cmet.2025.01.022","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.01.022","url":null,"abstract":"The liver is essential for normal fatty acid utilization during fasting. Circulating fatty acids are taken up by hepatocytes and esterified as triacylglycerols for either oxidative metabolization and ketogenesis or export. Whereas the regulation of fatty acid oxidation in hepatocytes is well understood, the uptake and retention of non-esterified fatty acids by hepatocytes is not. Here, we show that murine hepatic stellate cells (HSCs) and their abundantly expressed plasmalemma vesicle-associated protein (PLVAP) control hepatic substrate preference for fasting energy metabolism. HSC-specific ablation of PLVAP in mice elevated hepatic insulin signaling and improved glucose tolerance. Fasted HSC PLVAP knockout mice showed suppressed hepatic fatty acid esterification into di- and triacylglycerols, shifting fasting metabolism from fatty acid oxidation to reliance on carbohydrates. By super-resolution microscopy, we localized HSC PLVAP to caveolae residing along the sinusoidal lumen, supporting a role for HSCs and PLVAP-diaphragmed caveolae in normal fasting metabolism of the liver.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"84 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143532301","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
Pathogen-derived glyoxylate inhibits Tet2 DNA dioxygenase to facilitate bacterial persister formation 病原体衍生的乙醛酸抑制 Tet2 DNA 二氧酶，从而促进细菌宿主的形成
IF 29 1区 生物学
Cell metabolism Pub Date : 2025-03-03 DOI: 10.1016/j.cmet.2025.01.019
Zhou-Li Cheng, Shuyuan Zhang, Zhenning Wang, Aixia Song, Chao Gao, Jun-Bin Song, Pu Wang, Lei Zhang, Yue Zhou, Wenyan Shan, Chen Zhang, Jinye Zhang, Yiping Sun, Yanhui Xu, Fei Lan, Ming Zhong, Liang-Dong Lyu, Guanghua Huang, Fei Xavier Chen, Gang Li, Dan Ye
{"title":"Pathogen-derived glyoxylate inhibits Tet2 DNA dioxygenase to facilitate bacterial persister formation","authors":"Zhou-Li Cheng, Shuyuan Zhang, Zhenning Wang, Aixia Song, Chao Gao, Jun-Bin Song, Pu Wang, Lei Zhang, Yue Zhou, Wenyan Shan, Chen Zhang, Jinye Zhang, Yiping Sun, Yanhui Xu, Fei Lan, Ming Zhong, Liang-Dong Lyu, Guanghua Huang, Fei Xavier Chen, Gang Li, Dan Ye","doi":"10.1016/j.cmet.2025.01.019","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.01.019","url":null,"abstract":"Pathogenic bacterial persistence enables survival during antibiotic treatment, leading to treatment failure and recurrent infections, yet its underlying mechanisms remain unclear. Here, we reveal that glyoxylate, a metabolite originally evolved for alternative carbon utilization, functions as a signaling molecule to reprogram the host transcriptome and promote persister formation. Glyoxylate inhibits the DNA dioxygenase TET2, suppressing pro-inflammatory gene expression and attenuating host immune defense. Notably, stimulating TET2 activity with vitamin C or blocking glyoxylate production by <em>Salmonella</em> reduces bacterial antibiotic resistance and improves infection treatment outcomes. Beyond its metabolic role, glyoxylate emerges as a regulator of host-pathogen interactions, while TET2 plays a critical role in preventing bacterial persistence. Our findings suggest that targeting glyoxylate production or enhancing TET2 activity offers promising therapeutic strategies to combat bacterial persistence and enhance the efficacy of antibiotic treatments.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"37 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143532286","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
Realigned transsulfuration drives BRAF-V600E-targeted therapy resistance in melanoma 重组转硫驱动braf - v600e靶向治疗在黑色素瘤中的耐药性
IF 29 1区 生物学
Cell metabolism Pub Date : 2025-03-03 DOI: 10.1016/j.cmet.2025.01.021
Klaudia Borbényi-Galambos, Katalin Erdélyi, Tamás Ditrói, Eszter Petra Jurányi, Noémi Szántó, Réka Szatmári, Ágnes Czikora, Edward E. Schmidt, Dorottya Garai, Mihály Cserepes, Gabriella Liszkay, Erika Tóth, József Tóvári, Péter Nagy
{"title":"Realigned transsulfuration drives BRAF-V600E-targeted therapy resistance in melanoma","authors":"Klaudia Borbényi-Galambos, Katalin Erdélyi, Tamás Ditrói, Eszter Petra Jurányi, Noémi Szántó, Réka Szatmári, Ágnes Czikora, Edward E. Schmidt, Dorottya Garai, Mihály Cserepes, Gabriella Liszkay, Erika Tóth, József Tóvári, Péter Nagy","doi":"10.1016/j.cmet.2025.01.021","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.01.021","url":null,"abstract":"BRAF V600E-inhibition effectively treats melanoma, but acquired resistance rapidly develops. Protein expression profiles, mitochondrial energetics, metabolomics and fluxomics data in cell line, xenograft, and patient-derived xenograft systems revealed that concerted reprogramming of metabolic pathways (including glutaminolysis, glycolysis, TCA cycle, electron transport chain [ETC], and transsulfuration), along with an immediate cytoprotective response to drug-induced oxidative stress, underpins drug-tolerant persister cancer cell survival. Realignment of cysteine (Cys) metabolism, in particular an immediate upregulation of cystathionine-γ-lyase (CSE), was vital in persister cells. The oxidative cellular environment, drug-induced elevated cystine uptake and oxidative Cys catabolism, increased intracellular cystine/Cys ratios, thereby favoring cystine as a CSE substrate. This produces persulfides and hydrogen sulfide to protect protein thiols and support elevated energy demand in persister cells. Combining BRAF V600E inhibitors with CSE inhibitors effectively diminished proliferative relapse in culture models and increased progression-free survival of xenografted mice. This, together with induced CSE expression in patient samples under BRAF-V600E-inhibition, reveals an approach to increase BRAF-V600E-targeted therapeutic efficacy.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"34 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143532400","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
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