Cell metabolismPub Date : 2025-04-22DOI: 10.1016/j.cmet.2025.04.001
Yuki Tatekoshi, Amir Mahmoodzadeh, Jason S. Shapiro, Mingyang Liu, George M. Bianco, Ayumi Tatekoshi, Spencer Duncan Camp, Adam De Jesus, Navid Koleini, Santiago De La Torre, J. Andrew Wasserstrom, Wolfgang H. Dillmann, Benjamin R. Thomson, Kenneth C. Bedi, Kenneth B. Margulies, Samuel E. Weinberg, Hossein Ardehali
{"title":"Protein O-GlcNAcylation and hexokinase mitochondrial dissociation drive heart failure with preserved ejection fraction","authors":"Yuki Tatekoshi, Amir Mahmoodzadeh, Jason S. Shapiro, Mingyang Liu, George M. Bianco, Ayumi Tatekoshi, Spencer Duncan Camp, Adam De Jesus, Navid Koleini, Santiago De La Torre, J. Andrew Wasserstrom, Wolfgang H. Dillmann, Benjamin R. Thomson, Kenneth C. Bedi, Kenneth B. Margulies, Samuel E. Weinberg, Hossein Ardehali","doi":"10.1016/j.cmet.2025.04.001","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.04.001","url":null,"abstract":"Heart failure with preserved ejection fraction (HFpEF) is a common cause of morbidity and mortality worldwide, but its pathophysiology remains unclear. Here, we report a mouse model of HFpEF and show that hexokinase (HK)-1 mitochondrial binding in endothelial cells (ECs) is critical for protein O-GlcNAcylation and the development of HFpEF. We demonstrate increased mitochondrial dislocation of HK1 within ECs in HFpEF mice. Mice with deletion of the mitochondrial-binding domain of HK1 spontaneously develop HFpEF and display impaired angiogenesis. Spatial proximity of dislocated HK1 and O-linked N-acetylglucosamine transferase (OGT) causes increased OGT activity, shifting the balance of the hexosamine biosynthetic pathway intermediates into the O-GlcNAcylation machinery. EC-specific overexpression of O-GlcNAcase and an OGT inhibitor reverse angiogenic defects and the HFpEF phenotype, highlighting the importance of protein O-GlcNAcylation in the development of HFpEF. Our study demonstrates a new mechanism for HFpEF through HK1 cellular localization and resultant protein O-GlcNAcylation, and provides a potential therapy for HFpEF.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"62 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143857785","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 : 2025-04-22DOI: 10.1016/j.cmet.2025.03.017
Cuauhtemoc B. Ramirez, In Sook Ahn, Varvara I. Rubtsova, Ingrid Cely, Johnny Le, Joohwan Kim, Sunhee Jung, Miranda E. Kelly, Yeojin Kim, Hosung Bae, Won-Suk Song, Yasmine H. Alam, Guanglin Zhang, Graciel Diamante, Alina Chao, Lauren Hoffner, Alexis Anica, Izabelle Le, Miranda L. Lopez, Ian J. Tamburini, Cholsoon Jang
{"title":"Circulating glycerate predicts resilience to fructose-induced hepatic steatosis","authors":"Cuauhtemoc B. Ramirez, In Sook Ahn, Varvara I. Rubtsova, Ingrid Cely, Johnny Le, Joohwan Kim, Sunhee Jung, Miranda E. Kelly, Yeojin Kim, Hosung Bae, Won-Suk Song, Yasmine H. Alam, Guanglin Zhang, Graciel Diamante, Alina Chao, Lauren Hoffner, Alexis Anica, Izabelle Le, Miranda L. Lopez, Ian J. Tamburini, Cholsoon Jang","doi":"10.1016/j.cmet.2025.03.017","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.03.017","url":null,"abstract":"Excessive intake of dietary fructose increases the risk of metabolic-dysfunction-associated steatotic liver disease (MASLD), cirrhosis, and cancers. However, what host factors determine disease vulnerability is incompletely understood. Here, we leverage genetically divergent mouse strains, mass spectrometry-based metabolomics, and <em>in vivo</em> isotope tracing, identifying circulating glycerate as a biomarker that predicts resilience to fructose-induced hepatic steatosis in both sexes. We found that the surge of circulating glycerate after an oral fructose provision reflects strong small-intestinal fructose catabolism. Such fructose clearance by the small intestine is linked to a weaker induction of hepatic <em>de novo</em> lipogenesis and steatosis upon chronic fructose exposure across strains. These data indicate the potential utility of an oral fructose tolerance test and circulating glycerate measurements to predict an individual's susceptibility to fructose-elicited steatotic liver and provide personalized dietary recommendations.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"35 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143857781","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 : 2025-04-16DOI: 10.1016/j.cmet.2025.03.015
Baiyu He, Kyle D. Copps, Oliver Stöhr, Beikl Liu, Songhua Hu, Shakchhi Joshi, Marcia C. Haigis, Morris F. White, Hao Zhu, Rongya Tao
{"title":"Spatial regulation of glucose and lipid metabolism by hepatic insulin signaling","authors":"Baiyu He, Kyle D. Copps, Oliver Stöhr, Beikl Liu, Songhua Hu, Shakchhi Joshi, Marcia C. Haigis, Morris F. White, Hao Zhu, Rongya Tao","doi":"10.1016/j.cmet.2025.03.015","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.03.015","url":null,"abstract":"Hepatic insulin sensitivity is critical for systemic glucose and lipid homeostasis. The liver is spatially organized into zones in which hepatocytes express distinct metabolic enzymes; however, the functional significance of this zonation to metabolic dysregulation caused by insulin resistance is undetermined. Here, we used CreER mice to selectively disrupt insulin signaling in periportal (PP) and pericentral (PC) hepatocytes. PP-insulin resistance has been suggested to drive combined hyperglycemia and excess lipogenesis in individuals with type 2 diabetes. However, PP-insulin resistance in mice impaired lipogenesis and suppressed high-fat diet (HFD)-induced hepatosteatosis, despite elevated gluconeogenesis and insulin. In contrast, PC-insulin resistance reduced HFD-induced PC steatosis while preserving normal glucose homeostasis, in part by shifting glycolytic metabolism from the liver to the muscle. These results demonstrate distinct roles of insulin in PP versus PC hepatocytes and suggest that PC-insulin resistance might be therapeutically useful to combat hepatosteatosis without compromising glucose homeostasis.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"21 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143837037","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 : 2025-04-14DOI: 10.1016/j.cmet.2025.03.014
Xinxin Song, Zhuan Zhou, Jiao Liu, Jingbo Li, Chunhua Yu, Herbert J. Zeh, Daniel J. Klionsky, Brent R. Stockwell, Jiayi Wang, Rui Kang, Guido Kroemer, Daolin Tang
{"title":"Cytosolic cytochrome c represses ferroptosis","authors":"Xinxin Song, Zhuan Zhou, Jiao Liu, Jingbo Li, Chunhua Yu, Herbert J. Zeh, Daniel J. Klionsky, Brent R. Stockwell, Jiayi Wang, Rui Kang, Guido Kroemer, Daolin Tang","doi":"10.1016/j.cmet.2025.03.014","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.03.014","url":null,"abstract":"The release of cytochrome <em>c</em>, somatic (CYCS) from mitochondria to the cytosol is an established trigger of caspase-dependent apoptosis. Here, we unveil an unexpected role for cytosolic CYCS in inhibiting ferroptosis—a form of oxidative cell death driven by uncontrolled lipid peroxidation. Mass spectrometry and site-directed mutagenesis revealed the existence of a cytosolic complex composed of inositol polyphosphate-4-phosphatase type I A (INPP4A) and CYCS. This CYCS-INPP4A complex is distinct from the CYCS-apoptotic peptidase activating factor 1 (APAF1)-caspase-9 apoptosome formed during mitochondrial apoptosis. CYCS boosts INPP4A activity, leading to increased formation of phosphatidylinositol-3-phosphate, which prevents phospholipid peroxidation and plasma membrane rupture, thus averting ferroptotic cell death. Unbiased screening led to the identification of the small-molecule compound 10A3, which disrupts the CYCS-INPP4A interaction. 10A3 sensitized cultured cells and tumors implanted in immunocompetent mice to ferroptosis. Collectively, these findings redefine our understanding of cytosolic CYCS complexes that govern diverse cell death pathways.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"6 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143827149","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 : 2025-04-11DOI: 10.1016/j.cmet.2025.03.013
Ludovica Cotellessa, Veronica Sobrino, Mauro S.B. Silva, Maxime Delit, Hélène Maitre, Emilie Caron, Gaëtan Ternier, Natalia da Silva Lima, Tori Lhomme, Frank Giton, Andrea Sorrentino, Laura Carraresi, Giovanna Di Nardo, Ruben Nogueiras, Manuel Tena-Sempere, Vincent Prevot, Paolo Giacobini
{"title":"Preventing and correcting polycystic ovary syndrome by targeting anti-Müllerian hormone signaling in minipuberty and adulthood in mice","authors":"Ludovica Cotellessa, Veronica Sobrino, Mauro S.B. Silva, Maxime Delit, Hélène Maitre, Emilie Caron, Gaëtan Ternier, Natalia da Silva Lima, Tori Lhomme, Frank Giton, Andrea Sorrentino, Laura Carraresi, Giovanna Di Nardo, Ruben Nogueiras, Manuel Tena-Sempere, Vincent Prevot, Paolo Giacobini","doi":"10.1016/j.cmet.2025.03.013","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.03.013","url":null,"abstract":"Polycystic ovary syndrome (PCOS), the most common endocrinopathy in women, causes significant reproductive and metabolic comorbidities, with no current cure. Gestational androgen and anti-Müllerian hormone (AMH) excess are linked to PCOS, and prenatal aberrant exposure to these hormones induces PCOS-like traits in animal models. However, whether the AMH effects on PCOS programming could extend to early postnatal life remains unknown. Clinical observations showed higher AMH levels during minipuberty in infants of mothers with PCOS, but whether this contributes to PCOS development is uncertain. Here, we show that exposure to high AMH levels during minipuberty in mice causes PCOS-like reproductive and metabolic defects in both sexes. A neutralizing antibody targeting AMH receptor 2 (AMHR2) prevented these defects when administered during minipuberty and alleviated symptoms when given in adulthood. These findings highlight the causal role of elevated AMH in PCOS and suggest AMHR2-targeting therapy as a potential preventive or curative approach.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"0 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819965","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}
{"title":"Targeted tumor therapy with L-cyst(e)ine-addicted bacteria-nanodrug biohybrids","authors":"Yu-Zhang Wang, Wei-Hai Chen, Zi-Yi Han, Shi-Man Zhang, Ping Ji, Cheng Zhang, Jun-Long Liang, Xian-Zheng Zhang","doi":"10.1016/j.cmet.2025.03.012","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.03.012","url":null,"abstract":"Bacteria-based metabolic therapy has been acknowledged as a promising strategy for tumor treatment. However, the insufficient efficiency of wild-type bacteria severely restricts their therapeutic efficacy. Here, we elaborately develop an ʟ-cyst(e)ine-addicted bacteria-nanodrug biohybrid for metabolic therapy through a dual-selection directed evolution strategy. Our evolved strain exhibits a 36-fold increase in ʟ-cystine uptake and a 23-fold improvement in total activity of cysteine desulfhydrases compared with the wild-type strain. By conjugating with DMXAA-loaded liposomes, the engineered bacteria-nanodrug biohybrid not only prevents the influx of nutrients into the tumor by blocking neovasculature but also achieves efficient and durable CySS catabolism locally. The unavailable of Cys species disrupts redox homeostasis and strikingly increases intracellular ROS level, achieving favorable therapeutic outcomes in multiple tumor models. Our study not only highlights the promise of directed evolution strategy in enhancing the stability and efficiency of bacteria-based living biocatalyst but also provides new opportunities for antitumor metabolic therapy.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"43 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143814003","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 : 2025-04-08DOI: 10.1016/j.cmet.2025.03.011
Eric Ravussin, Guillermo Sanchez-Delgado, Corby K. Martin, Robbie A. Beyl, Frank L. Greenway, Libbey S. O’Farrell, William C. Roell, Hui-Rong Qian, Jing Li, Hiroshi Nishiyama, Axel Haupt, Edward J. Pratt, Shweta Urva, Zvonko Milicevic, Tamer Coskun
{"title":"Tirzepatide did not impact metabolic adaptation in people with obesity, but increased fat oxidation","authors":"Eric Ravussin, Guillermo Sanchez-Delgado, Corby K. Martin, Robbie A. Beyl, Frank L. Greenway, Libbey S. O’Farrell, William C. Roell, Hui-Rong Qian, Jing Li, Hiroshi Nishiyama, Axel Haupt, Edward J. Pratt, Shweta Urva, Zvonko Milicevic, Tamer Coskun","doi":"10.1016/j.cmet.2025.03.011","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.03.011","url":null,"abstract":"Tirzepatide, a glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 receptor agonist, promoted significant body weight reduction in the phase 3 clinical trials. We conducted a preclinical study and a phase 1 clinical trial (NCT04081337) to understand potential mechanisms mediating tirzepatide-induced weight loss in mice and people with obesity. In calorie-restricted, obese mice, chronic treatment with tirzepatide reduced the drop in energy expenditure that occurred in vehicle-treated and pair-fed mice, indicating that tirzepatide attenuated metabolic adaptation. Respiratory exchange ratio also decreased in tirzepatide-treated mice, indicating increased fat oxidation. In the clinical trial, tirzepatide appeared to have no impact on metabolic adaptation but led to increased fat oxidation and reductions in appetite and calorie intake during an <em>ad libitum</em> test meal (vs. placebo). This is the first study to provide insights into the mechanisms of action of tirzepatide on weight loss with respect to calorie intake, energy expenditure, and macronutrient utilization.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"18 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143798388","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 : 2025-04-07DOI: 10.1016/j.cmet.2025.03.009
Christopher Auger, Mark Li, Masanori Fujimoto, Kenji Ikeda, Jin-Seon Yook, Timothy R. O’Leary, María Paula Huertas Caycedo, Cai Xiaohan, Satoshi Oikawa, Anthony R.P. Verkerke, Kosaku Shinoda, Patrick R. Griffin, Kenji Inaba, Roland H. Stimson, Shingo Kajimura
{"title":"Identification of a molecular resistor that controls UCP1-independent Ca2+ cycling thermogenesis in adipose tissue","authors":"Christopher Auger, Mark Li, Masanori Fujimoto, Kenji Ikeda, Jin-Seon Yook, Timothy R. O’Leary, María Paula Huertas Caycedo, Cai Xiaohan, Satoshi Oikawa, Anthony R.P. Verkerke, Kosaku Shinoda, Patrick R. Griffin, Kenji Inaba, Roland H. Stimson, Shingo Kajimura","doi":"10.1016/j.cmet.2025.03.009","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.03.009","url":null,"abstract":"Adipose tissue thermogenesis contributes to energy balance via mitochondrial uncoupling protein 1 (UCP1) and UCP1-independent pathways. Among UCP1-independent thermogenic mechanisms, one involves Ca<sup>2+</sup> cycling via SERCA2b in adipose tissue; however, the underlying molecular basis remains elusive. Here, we report that an endoplasmic reticulum (ER) membrane-anchored peptide, C4orf3 (also known as another regulin [ALN]), uncouples SERCA2b Ca<sup>2+</sup> transport from its ATP hydrolysis, rendering the SERCA2b-C4orf3 complex exothermic. Loss of C4orf3/ALN improved the energetic efficiency of SERCA2b-dependent Ca<sup>2+</sup> transport without affecting SERCA2 expression, thereby reducing adipose tissue thermogenesis and increasing the adiposity of mice. Notably, genetic depletion of <em>C4orf3</em> resulted in compensatory activation of UCP1-dependent thermogenesis following cold challenge. We demonstrated that genetic loss of both <em>C4orf3</em> and <em>Ucp1</em> additively impaired cold tolerance <em>in vivo</em>. Together, this study identifies C4orf3 as the molecular resistor to SERCA2b-mediated Ca<sup>2+</sup> import that plays a key role in UCP1-independent thermogenesis and energy balance.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"31 Suppl 9 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143789765","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 : 2025-04-07DOI: 10.1016/j.cmet.2025.03.003
Seyedeh Sahar Mortazavi Farsani, Jignesh Soni, Lu Jin, Anil Kumar Yadav, Shivani Bansal, Tian Mi, Leena Hilakivi-Clarke, Robert Clarke, Benjamin Youngblood, Amrita Cheema, Vivek Verma
{"title":"Pyruvate kinase M2 activation reprograms mitochondria in CD8 T cells, enhancing effector functions and efficacy of anti-PD1 therapy","authors":"Seyedeh Sahar Mortazavi Farsani, Jignesh Soni, Lu Jin, Anil Kumar Yadav, Shivani Bansal, Tian Mi, Leena Hilakivi-Clarke, Robert Clarke, Benjamin Youngblood, Amrita Cheema, Vivek Verma","doi":"10.1016/j.cmet.2025.03.003","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.03.003","url":null,"abstract":"Mitochondria regulate T cell functions and response to immunotherapy. We show that pyruvate kinase M2 (PKM2) activation enhances mitochondria-dependent effector functions in CD8 and chimeric antigen receptor (CAR)-T cells. Multi-omics and <sup>13</sup>C-glucose tracer studies showed that PKM2 agonism alters one-carbon metabolism, decreasing methionine levels, resulting in hypomethylated nuclear and mitochondrial DNA and enhancing mitochondrial biogenesis and functions. PKM2 activation increased the recall responses and anti-tumor functions of CD8 T cells, enhancing adoptive cell therapy. In preclinical models, the PKM2 agonist induced CD8 T cell-dependent anti-tumor responses that synergized with anti-programmed death 1 (PD1) therapy. Immunologically, PKM2 agonists boosted the activation of effector T cells while reducing FoxP3<sup>+</sup> T regulatory (Treg) cells in the tumors. The anti-PD1 combination enhanced the frequency of tumor-specific activated CD8 T cells. Together, PKM2 agonism increased mitochondrial functions supporting cell cytotoxicity. Hence, pharmacological targeting of PKM2 can be a clinically viable strategy for enhancement of adoptive cell therapy, <em>in situ</em> anti-tumor immune responses, and immune checkpoint blockade therapy.<h3>Video abstract</h3><span><span><span><span><video controls=\"\" crossorigin=\"anonymous\" data-counter-fields='{\"currObj\":\"MiamiMultiMediaURL\",\"activity\":\"playButton\",\"MMCType\":\"mp4\",\"eid\":\"1-s2.0-S1550413125001068-mmc3.mp4\"}' poster=\"https://ars.els-cdn.com/content/image/1-s2.0-S1550413125001068-mmc3.jpg\" preload=\"auto\" style=\"width:100%\"><source src=\"https://ars.els-cdn.com/content/image/1-s2.0-S1550413125001068-mmc3.mp4\" type=\"video/mp4\"/></video></span><span><span>Download: <span>Download video (57MB)</span></span></span></span></span></span>","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"59 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143789764","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}
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
