Cell metabolismPub Date : 2026-01-06DOI: 10.1016/j.cmet.2025.12.001
David S. Ludwig
{"title":"Confusion about energy and energy density in a 3-week trial of ultra-processed food","authors":"David S. Ludwig","doi":"10.1016/j.cmet.2025.12.001","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.12.001","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Main text</h2>The complexity of nutrition and human behavior poses a major challenge to the study of diet-disease relationships, prompting some researchers to adopt a feeding study design. Conceptually, feeding studies provide an opportunity to isolate the effects of a single dietary factor of interest, controlling for confounding influences. Toward this end, Preston et al.<sup>1</sup> conducted a macronutrient-controlled 2-by-2 cross-over feeding trial comparing an ultra-processed food (UPF) diet with an “unprocessed”</section></section><section><section><h2>Acknowledgments</h2>This work was done without financial sponsorship.</section></section><section><section><h2>Declaration of interests</h2>D.S.L. received royalties for books on obesity and nutrition that recommend a reduced glycemic load diet.</section></section>","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"29 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145902688","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 : 2026-01-06DOI: 10.1016/j.cmet.2025.11.017
Ioannis G. Lempesis, Frank A.J.L. Scheer
{"title":"Illuminating the influence of natural daylight on human metabolism","authors":"Ioannis G. Lempesis, Frank A.J.L. Scheer","doi":"10.1016/j.cmet.2025.11.017","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.11.017","url":null,"abstract":"Humankind currently lives largely under artificial light, potentially negatively impacting circadian-metabolic alignment and predisposing it to diseases. Harmsen et al.<span><span><sup>1</sup></span></span> show that natural daylight exposure during office hours improves several metabolic parameters including glucose regulation, enhancing fat oxidation, and advancing muscle-clock circadian phase in individuals with type 2 diabetes.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"57 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2026-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145907940","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 : 2025-12-19DOI: 10.1016/j.cmet.2025.11.012
María Ángeles Cáliz-Molina, Raúl López-Fernández-Sobrino, Inmaculada Pino-Pérez, Concepción Panadero-Morón, María del Carmen Vilches-Pérez, María Camacho-Cabrera, Almudena García-Ruiz, Leopoldo Pérez-Rosendo, Isabel Espadas, Alejandro Sola-García, Mario Soriano-Navarro, Franz Martin, Mónica Venegas-Calerón, Joaquín Jesús Salas, Enrique Martínez-Force, Luis C. Romero, Ángeles Aroca, Román González-Prieto, Máximo Bernabeu-Wittel, Vivian Capilla-González, Christopher Hine, Alejandro Martín-Montalvo
{"title":"Enhanced non-enzymatic H2S generation extends lifespan and healthspan in male mice","authors":"María Ángeles Cáliz-Molina, Raúl López-Fernández-Sobrino, Inmaculada Pino-Pérez, Concepción Panadero-Morón, María del Carmen Vilches-Pérez, María Camacho-Cabrera, Almudena García-Ruiz, Leopoldo Pérez-Rosendo, Isabel Espadas, Alejandro Sola-García, Mario Soriano-Navarro, Franz Martin, Mónica Venegas-Calerón, Joaquín Jesús Salas, Enrique Martínez-Force, Luis C. Romero, Ángeles Aroca, Román González-Prieto, Máximo Bernabeu-Wittel, Vivian Capilla-González, Christopher Hine, Alejandro Martín-Montalvo","doi":"10.1016/j.cmet.2025.11.012","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.11.012","url":null,"abstract":"","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"37 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145784404","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 : 2025-12-18DOI: 10.1016/j.cmet.2025.11.006
Jan-Frieder Harmsen, Ivo Habets, Andrew D. Biancolin, Agata Lesniewska, Nicholas E. Phillips, Loic Metz, Juan Sanchez-Avila, Marit Kotte, Merel Timmermans, Dzhansel Hashim, Soraya S. de Kam, Gert Schaart, Johanna A. Jörgensen, Anne Gemmink, Esther Moonen-Kornips, Daniel Doligkeit, Tineke van de Weijer, Mijke Buitinga, Florian Haans, Rebecca De Lorenzo, Joris Hoeks
{"title":"Natural daylight during office hours improves glucose control and whole-body substrate metabolism","authors":"Jan-Frieder Harmsen, Ivo Habets, Andrew D. Biancolin, Agata Lesniewska, Nicholas E. Phillips, Loic Metz, Juan Sanchez-Avila, Marit Kotte, Merel Timmermans, Dzhansel Hashim, Soraya S. de Kam, Gert Schaart, Johanna A. Jörgensen, Anne Gemmink, Esther Moonen-Kornips, Daniel Doligkeit, Tineke van de Weijer, Mijke Buitinga, Florian Haans, Rebecca De Lorenzo, Joris Hoeks","doi":"10.1016/j.cmet.2025.11.006","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.11.006","url":null,"abstract":"Because 80%–90% of our time is spent indoors and daylight is the main synchronizer of the central biological clock, the chronic lack of daylight is increasingly considered as a risk factor for metabolic diseases, such as type 2 diabetes. In a randomized crossover design (NCT05263232), 13 individuals with type 2 diabetes were exposed to natural daylight facilitated through windows vs. constant artificial lighting during office hours for 4.5 consecutive days. Continuous glucose monitoring revealed that participants spent more time in the normal glucose range, and whole-body substrate metabolism shifted toward a greater reliance on fat oxidation during daylight. Primary myotubes cultured from skeletal muscle biopsies displayed a phase advance after daylight exposure. Multi-omic analyses revealed daylight-induced differences in serum metabolites, lipids, and monocyte transcripts. Our findings suggest that natural daylight exposure has a positive metabolic impact on individuals with type 2 diabetes and could support the treatment of metabolic diseases.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"7 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145778081","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 : 2025-12-11DOI: 10.1016/j.cmet.2025.11.010
Alvin P. Chan, Kelsey E. Jarrett, Rochelle W. Lai, Madelaine C. Brearley-Sholto, Angela S. Cheng, Maria O. Taveras, Anne M. Iwata, Michelle E. Steel, Andrew Lau, Emily C. Whang, John P. Kennelly, Yajing Gao, Gabriella E. Rubert, Heidi M. Schmidt, Emily P. Smith, Baolong Su, Kevin J. Williams, Elizabeth J. Tarling, Thomas Q. de Aguiar Vallim
{"title":"Bile acids regulate lipid metabolism through selective actions on fatty acid absorption","authors":"Alvin P. Chan, Kelsey E. Jarrett, Rochelle W. Lai, Madelaine C. Brearley-Sholto, Angela S. Cheng, Maria O. Taveras, Anne M. Iwata, Michelle E. Steel, Andrew Lau, Emily C. Whang, John P. Kennelly, Yajing Gao, Gabriella E. Rubert, Heidi M. Schmidt, Emily P. Smith, Baolong Su, Kevin J. Williams, Elizabeth J. Tarling, Thomas Q. de Aguiar Vallim","doi":"10.1016/j.cmet.2025.11.010","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.11.010","url":null,"abstract":"Intestinal lipid absorption, the entry point for fats into the body, requires the coordinated actions of bile acids and lipases. Here, we uncover distinct yet cooperative roles of bile acids in driving the differential uptake of dietary fatty acids. We first decreased the bile acid pool size by disrupting the rate-limiting enzyme in bile acid synthesis, <em>Cyp7a1</em>, using liver-directed gene editing in mice. Compared with lipase inhibition, reduced bile acids prevented diet-induced obesity, increased anorectic hormones, suppressed excessive eating, and improved systemic lipid metabolism. Remarkably, decreasing bile acids selectively reduced the absorption of saturated fatty acids but preserved polyunsaturated fatty acids. By targeting additional bile acid enzymes, we identified specific functions of individual bile acid species. Mechanistically, we show that cholic acid preferentially solubilizes polyunsaturated fatty acids into mixed micelles for intestinal uptake. Our studies demonstrate that bile acids can selectively control fatty acid uptake, revealing insights for future interventions in metabolic diseases.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"10 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145728734","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":"Macrophage PD-1 regulates energy expenditure and metabolic dysfunction under immune checkpoint blockade","authors":"Ming-Ming Wu, Yan-Chao Yang, Zhi-Qiang Hu, Jie-Yu Chang, Han Xiao, Chang Miao, Bo-Wen Zhang, Zhi-Xi He, Di Zhu, Yu-Ran Duan, Shuo Wang, Jian-Yu Liu, Zhan-Peng Guo, Yu Sun, Dan-Yang Liu, Miao Yu, Yue Zhang, Jian-Jun Mao, Shuai Jiang, Bing-Kun Zhang, Zhu Mei, Jun Gao, Chen Liang, Qiu-Shi Wang, Chang-Jiang Yu, Dan Zhao, Cheng-Hui Yan, Yue Li, Zhen-Wei Pan, Zheng Chen, Da-Qian Xu, Tong Liu, Yong Ji, Zhi-Ren Zhang","doi":"10.1016/j.cmet.2025.11.009","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.11.009","url":null,"abstract":"Immune checkpoint inhibitor (ICI) therapies increase the risk of metabolic syndrome; the underlying mechanisms remain elusive. We show that an anti-PD-1 antibody targets macrophage PD-1 to reduce energy expenditure without affecting food intake, augmenting the susceptibility of mice to high-fat diet (HFD)-induced obesity and systemic metabolic disorders. Mechanistically, lipopolysaccharide (LPS) activates Unc-51-like autophagy activating kinase 1 (ULK1) in a mammalian target of rapamycin (mTOR)-dependent manner. Activated ULK1 phosphorylates PD-1 at Thr250 to inhibit FBXO38-mediated PD-1 ubiquitination and degradation by disrupting FBXO38-PD-1 binding. Phosphorylated PD-1 interacts with inositol-requiring enzyme 1α (IRE1α) and attenuates IRE1α autophosphorylation to suppress endoplasmic reticulum (ER) stress-mediated inflammatory responses. Suppressing IRE1α alleviates HFD-induced metabolic disorders in macrophage-specific PD-1 knockout mice by rescuing the reduced energy expenditure. Our findings highlight the critical role of macrophage PD-1 at the intersection of immune checkpoint blockade, energy expenditure, and metabolic dysfunction. The underscored moonlighting function of macrophage PD-1 may provide a new rationale for combating ICI therapy- and HFD-induced metabolic diseases.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"148 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145731565","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 : 2025-12-05DOI: 10.1016/j.cmet.2025.11.007
Jian Gao, Wei Zhang, Qian Li, Dan Zhao, Jiayi Cai, Qing Wang, Xin Li, Tingting Liu, Jin Li, Wengan Xiao, Huimin Li, Min Du, Bing Zhang, Peiying Li, Hong Tu, Yu Gan
{"title":"Restricting lipid accumulation in tumor-infiltrating neutrophils mediates caloric restriction-induced anti-cancer effects","authors":"Jian Gao, Wei Zhang, Qian Li, Dan Zhao, Jiayi Cai, Qing Wang, Xin Li, Tingting Liu, Jin Li, Wengan Xiao, Huimin Li, Min Du, Bing Zhang, Peiying Li, Hong Tu, Yu Gan","doi":"10.1016/j.cmet.2025.11.007","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.11.007","url":null,"abstract":"Caloric restriction (CR) induces tumor resistance in mammals, but its mechanisms remain poorly understood. Here, we found that CR altered the proportions and gene expression profiles of tumor-infiltrating neutrophils (TINs). Depletion of neutrophils largely abrogated CR-induced tumor inhibition across multiple murine cancer models, underscoring their critical role in CR’s broad anti-tumor effect. CR-induced gene expression changes in TINs were associated primarily with lipid-related processes, notably downregulating hypoxia-inducible lipid droplet-associated (HILPDA). This downregulation reduced lipid accumulation in TINs, limiting tumor growth and enhancing anti-tumor immunity by decreasing lipid transfer to tumor and immune effector cells. Upstream, CR reduced hypoxia-inducible factor 1 (HIF-1α) mRNA expression in circulating neutrophils by decreasing insulin-like growth factor 1 (IGF-1), thereby limiting HILPDA expression in TINs. Patients with lung cancer who had low baseline neutrophil HIF-1α mRNA exhibited improved responses to combined immunotherapy. These findings identify a novel neutrophil- and lipid-centered mechanism for CR-induced tumor inhibition, suggesting the IGF-1/HIF-1α/HILPDA axis as a therapeutic target.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"52 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145689055","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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