Cell metabolism最新文献_第3页

Testing the carbohydrate-insulin model: The data are supportive! 测试碳水化合物-胰岛素模型：数据是支持的！

IF 29 1区生物学

Cell metabolism Pub Date : 2025-06-03 DOI: 10.1016/j.cmet.2025.04.010

David S. Ludwig, Jennie C. Brand-Miller, Cara B. Ebbeling, Mark I. Friedman, Nicholas G. Norwitz, Adrian Soto-Mota

{"title":"Testing the carbohydrate-insulin model: The data are supportive!","authors":"David S. Ludwig, Jennie C. Brand-Miller, Cara B. Ebbeling, Mark I. Friedman, Nicholas G. Norwitz, Adrian Soto-Mota","doi":"10.1016/j.cmet.2025.04.010","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.04.010","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Main text</h2>Mean body weight continues to rise worldwide despite intensive prevention and treatment focused on energy restriction, leading to formulation of new models of obesity pathogenesis. In the carbohydrate-insulin model (CIM),<sup>1</sup> a diet high in glycemic load (GL) (the multiplicative product of glycemic index [GI] and carbohydrate amount) initiates a sequence of hormonal responses that shift substrate partitioning<sup>2</sup> toward energy storage and away from oxidation in lean tissues. Thus, the CIM provides an</section></section><section><section><h2>Acknowledgments</h2>This work was done without financial sponsorship.</section></section><section><section><h2>Declaration of interests</h2>J.B.M. is a co-author of books based on the glycemic index of foods, oversees a glycemic index testing service at the University of Sydney, and is a consultant for the China National Research Institute of Food and Fermentation Industries, the Novo Foundation, and Zoe Global. She was President of the Glycemic Index Foundation from 2002 to 2024. D.S.L received royalties for books on obesity and nutrition that recommend a reduced-glycemic load diet. N.G.N. received royalties for a ketogenic diet</section></section>","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"4 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144202290","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

CROSsing the Rubicon: Brainstem peroxide levels drive sleep-wake dynamics 跨越卢比孔河：脑干过氧化氢水平驱动睡眠-觉醒动力学

IF 29 1区生物学

Cell metabolism Pub Date : 2025-06-03 DOI: 10.1016/j.cmet.2025.05.005

Nicole M. Gilette, Jonathan O. Lipton

引用次数: 0

Monoclonal antibody therapy for PCOS? 单克隆抗体治疗多囊卵巢综合征？

IF 29 1区生物学

Cell metabolism Pub Date : 2025-06-03 DOI: 10.1016/j.cmet.2025.05.002

David H. Abbott, Daniel A. Dumesic

引用次数: 0

Nicotinic acid riboside maintains NAD+ homeostasis and ameliorates aging-associated NAD+ decline 烟酸核糖体维持NAD+体内平衡并改善与衰老相关的NAD+下降

IF 29 1区生物学

Cell metabolism Pub Date : 2025-05-22 DOI: 10.1016/j.cmet.2025.05.004

Won-Suk Song, Xiyu Shen, Kang Du, Cuauhtemoc B. Ramirez, Sang Hee Park, Yang Cao, Johnny Le, Hosung Bae, Joohwan Kim, Yujin Chun, Nikki Joyce Khong, Marie Kim, Sunhee Jung, Wonsuk Choi, Miranda L. Lopez, Zaid Said, Zehan Song, Sang-Guk Lee, Dequina Nicholas, Yo Sasaki, Qin Yang

引用次数: 0

Dietary-timing-induced gut microbiota diurnal oscillations modulate inflammatory rhythms in rheumatoid arthritis 饮食时间诱导的肠道微生物群昼夜振荡调节类风湿关节炎的炎症节律

IF 29 1区生物学

Cell metabolism Pub Date : 2025-05-22 DOI: 10.1016/j.cmet.2025.05.007

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

引用次数: 0

Semaglutide effects on energy balance are mediated by Adcyap1+ neurons in the dorsal vagal complex 半马鲁肽对能量平衡的影响是由迷走背复合体中的Adcyap1+神经元介导的

IF 29 1区生物学

Cell metabolism Pub Date : 2025-05-22 DOI: 10.1016/j.cmet.2025.04.018

Júlia Teixidor-Deulofeu, Sebastian Blid Sköldheden, Ferran Font-Gironès, Andrej Feješ, Johan Ruud, Linda Engström Ruud

{"title":"Semaglutide effects on energy balance are mediated by Adcyap1+ neurons in the dorsal vagal complex","authors":"Júlia Teixidor-Deulofeu, Sebastian Blid Sköldheden, Ferran Font-Gironès, Andrej Feješ, Johan Ruud, Linda Engström Ruud","doi":"10.1016/j.cmet.2025.04.018","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.04.018","url":null,"abstract":"The use of the GLP-1R agonist semaglutide is revolutionizing the treatment of obesity, yet its mechanistic effects on energy balance remain elusive. Here, we demonstrate that reactivation of semaglutide-responsive dorsal vagal complex neurons mimics the drug’s effects of reducing food intake and body weight and promoting fat utilization and conditioned taste aversion. We observe that many of the semaglutide-activated area postrema (AP) and nucleus of the solitary tract (NTS) neurons express <em>Adcyap1</em> mRNA, and ablation of AP/NTS <em>Adcyap1</em><sup>+</sup> neurons largely reverses semaglutide’s effects on energy balance acutely in lean mice and in subchronically treated obese mice. Semaglutide-activated AP/NTS <em>Adcyap1</em><sup>+</sup> neurons promote the loss of fat rather than lean mass, with only a modest effect on conditioned taste aversion. Furthermore, NTS <em>Adcyap1</em><sup>+</sup> neurons are engaged by GLP-1R-expressing AP neurons and are necessary for semaglutide-induced activation of several downstream satiety-related structures. Selective targeting of semaglutide-responsive <em>Adcyap1</em><sup>+</sup> neurons holds potential for improved future anti-obesity treatments.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"79 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144114385","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

Acetylated cellulose suppresses body mass gain through gut commensals consuming host-accessible carbohydrates 乙酰化纤维素通过肠道共生体消耗宿主可获得的碳水化合物来抑制体重增加

IF 29 1区生物学

Cell metabolism Pub Date : 2025-05-16 DOI: 10.1016/j.cmet.2025.04.013

Tadashi Takeuchi, Eiji Miyauchi, Yumiko Nakanishi, Yusuke Ito, Tamotsu Kato, Katsuki Yaguchi, Masami Kawasumi, Naoko Tachibana, Ayumi Ito, Shu Shimamoto, Akinobu Matsuyama, Nobuo Sasaki, Ikuo Kimura, Hiroshi Ohno

{"title":"Acetylated cellulose suppresses body mass gain through gut commensals consuming host-accessible carbohydrates","authors":"Tadashi Takeuchi, Eiji Miyauchi, Yumiko Nakanishi, Yusuke Ito, Tamotsu Kato, Katsuki Yaguchi, Masami Kawasumi, Naoko Tachibana, Ayumi Ito, Shu Shimamoto, Akinobu Matsuyama, Nobuo Sasaki, Ikuo Kimura, Hiroshi Ohno","doi":"10.1016/j.cmet.2025.04.013","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.04.013","url":null,"abstract":"Effective approaches to preventing and treating obesity are urgently needed. Although current strategies primarily focus on direct modulation of host metabolism, another promising approach may involve limiting nutrient availability through regulation of the gut microbiota, which links diet and host physiology. Here, we report that acetylated cellulose (AceCel), which markedly alters gut bacterial composition and function, reduces body mass gain in both wild-type and obese mice. AceCel limits carbohydrate oxidation and promotes fatty acid oxidation in the host liver in a microbiota-dependent manner. We further show that acetate enhances carbohydrate fermentation by the gut commensal <em>Bacteroides thetaiotaomicron</em>, depleting host-accessible simple sugars in the gut of AceCel-fed mice. These findings highlight the potential of AceCel as a prebiotic that regulates carbohydrate metabolism in both bacteria and host, offering promise as a therapeutic strategy for obesity.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"33 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144066028","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

Hydrogen peroxide in midbrain sleep neurons regulates sleep homeostasis 中脑睡眠神经元中的过氧化氢调节睡眠稳态

IF 29 1区生物学

Cell metabolism Pub Date : 2025-05-15 DOI: 10.1016/j.cmet.2025.04.016

Yujing Tian, Luwei Kang, Ngoc T. Ha, Juan Deng, Danqian Liu

{"title":"Hydrogen peroxide in midbrain sleep neurons regulates sleep homeostasis","authors":"Yujing Tian, Luwei Kang, Ngoc T. Ha, Juan Deng, Danqian Liu","doi":"10.1016/j.cmet.2025.04.016","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.04.016","url":null,"abstract":"Sleep could protect animals from oxidative damage, yet the dynamic interplay between the redox state and sleep homeostasis remains unclear. Here, we show that acute sleep deprivation (SD) in mice caused a general increase in brain oxidation, particularly in sleep-promoting regions. <em>In vivo</em> imaging of intracellular hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) real-time dynamics revealed that in nigra sleep neurons, the increase in cytosolic but not mitochondrial H<sub>2</sub>O<sub>2</sub> reflects sleep debt and tracks spontaneous wakefulness by positively correlating with wake duration. By controllably manipulating intraneuronal H<sub>2</sub>O<sub>2</sub>, we discovered that H<sub>2</sub>O<sub>2</sub> elevation is required for compensatory sleep and causally promotes sleep initiation, at least partly dependent on transient receptor potential melastatin 2 (TRPM2) channel. However, excessive H<sub>2</sub>O<sub>2</sub> induced brain inflammation and sleep fragmentation. Together, our study demonstrates intraneuronal H<sub>2</sub>O<sub>2</sub> as a crucial signaling molecule that translates brain redox imbalance into sleep drive and underscores the significance of oxidative eustress in sleep homeostasis.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"40 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980017","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 lipid remodeling in cold exposure uncovers direct regulation of bis(monoacylglycero)phosphate lipids by phospholipase A2 group XV 低温暴露时肝脏脂质重塑揭示了磷脂酶A2组XV对单酰基甘油磷酸脂的直接调节

IF 29 1区生物学

Cell metabolism Pub Date : 2025-05-14 DOI: 10.1016/j.cmet.2025.04.015

Jessica W. Davidson, Raghav Jain, Thomas Kizzar, Gisela Geoghegan, Daniel J. Nesbitt, Amy Cavanagh, Akira Abe, Kwamina Nyame, Andrea Hunger, Xiaojuan Chao, Isabella James, Helaina Walesewicz, Dominique A. Baldwin, Gina Wade, Sylwia Michorowska, Rakesh Verma, Kathryn Schueler, Vania Hinkovska-Galcheva, Evgenia Shishkova, Wen-Xing Ding, Judith A. Simcox

{"title":"Hepatic lipid remodeling in cold exposure uncovers direct regulation of bis(monoacylglycero)phosphate lipids by phospholipase A2 group XV","authors":"Jessica W. Davidson, Raghav Jain, Thomas Kizzar, Gisela Geoghegan, Daniel J. Nesbitt, Amy Cavanagh, Akira Abe, Kwamina Nyame, Andrea Hunger, Xiaojuan Chao, Isabella James, Helaina Walesewicz, Dominique A. Baldwin, Gina Wade, Sylwia Michorowska, Rakesh Verma, Kathryn Schueler, Vania Hinkovska-Galcheva, Evgenia Shishkova, Wen-Xing Ding, Judith A. Simcox","doi":"10.1016/j.cmet.2025.04.015","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.04.015","url":null,"abstract":"Cold exposure is a selective environmental stress that elicits a rapid metabolic shift to maintain energy homeostasis. In response to cold exposure, the liver rewires the metabolic state, shifting from glucose to lipid catabolism. By probing the liver lipids in cold exposure, we observed that the lysosomal bis(monoacylglycero)phosphate (BMP) lipids were rapidly increased during cold exposure. BMP lipid changes occurred independently of lysosomal abundance but were dependent on the lysosomal transcriptional regulator transcription factor EB (TFEB). Knockdown of <em>Tfeb</em> in hepatocytes decreased BMP lipid levels and led to cold intolerance in mice. We assessed TFEB-binding sites of lysosomal genes and determined that the phospholipase a2 group XV (PLA2G15) regulates BMP lipid catabolism. Decreasing <em>Pla2g15</em> levels in mice increased BMP lipids, ablated the cold-induced rise in BMP lipids, and improved cold tolerance. Mutation of the catalytic site of PLA2G15 ablated the BMP lipid breakdown. Together, our studies uncover TFEB regulation of BMP lipids through PLA2G15 catabolism.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"39 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143946252","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

FGF21 reverses MASH through coordinated actions on the CNS and liver FGF21通过对中枢神经系统和肝脏的协同作用逆转MASH

IF 29 1区生物学

Cell metabolism Pub Date : 2025-05-13 DOI: 10.1016/j.cmet.2025.04.014

Jesse P. Rose, Donald A. Morgan, Andrew I. Sullivan, Xiaorong Fu, Melissa Inigo-Vollmer, Shawn C. Burgess, David K. Meyerholz, Kamal Rahmouni, Matthew J. Potthoff

{"title":"FGF21 reverses MASH through coordinated actions on the CNS and liver","authors":"Jesse P. Rose, Donald A. Morgan, Andrew I. Sullivan, Xiaorong Fu, Melissa Inigo-Vollmer, Shawn C. Burgess, David K. Meyerholz, Kamal Rahmouni, Matthew J. Potthoff","doi":"10.1016/j.cmet.2025.04.014","DOIUrl":"https://doi.org/10.1016/j.cmet.2025.04.014","url":null,"abstract":"Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), represent a growing public health burden with limited therapeutic options. Recent studies have revealed that fibroblast growth factor 21 (FGF21)-based analogs can significantly improve MASH, but the mechanisms for this effect are not well understood. Here, we demonstrate that the beneficial metabolic effects of FGF21 to reverse MASH are mediated through distinct mechanisms to independently lower hepatic triglyceride and cholesterol levels. Specifically, FGF21 signaling directly to glutamatergic neurons in the central nervous system (CNS) stimulates hepatic triglyceride reduction and reversal of fibrosis, whereas FGF21 signaling directly to hepatocytes is necessary and sufficient to reduce hepatic cholesterol levels in mice. Mechanistically, we show that FGF21 acts in the CNS to increase sympathetic nerve activity to the liver, which suppresses hepatic <em>de novo</em> lipogenesis. These results provide critical insights into a promising pharmacological target to treat MASH.","PeriodicalId":9840,"journal":{"name":"Cell metabolism","volume":"41 1","pages":""},"PeriodicalIF":29.0,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143940143","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