Pub Date : 2026-01-20DOI: 10.1038/s42255-025-01435-2
Xun Huang, Li Ye
In this issue of Nature Metabolism, Neri et al. show that two distinct stellate ganglion subcircuits innervating interscapular brown adipose tissue (iBAT) separately control thermogenesis and glucose tolerance, providing a mechanistic explanation for temperature-independent benefits of iBAT on glycaemia.
{"title":"Heterogeneous sympathetic control of brown adipose tissue","authors":"Xun Huang, Li Ye","doi":"10.1038/s42255-025-01435-2","DOIUrl":"10.1038/s42255-025-01435-2","url":null,"abstract":"In this issue of Nature Metabolism, Neri et al. show that two distinct stellate ganglion subcircuits innervating interscapular brown adipose tissue (iBAT) separately control thermogenesis and glucose tolerance, providing a mechanistic explanation for temperature-independent benefits of iBAT on glycaemia.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"8 2","pages":"282-283"},"PeriodicalIF":20.8,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146005099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Psychological stress is increasingly linked to liver disease, but the underlying mechanisms remain unclear. Here we show that chronic stress disrupts a brain–liver circuit that impairs hepatic CD8+ T cell immunity and accelerates liver cancer progression. Using both oncogene-driven and carcinogen-driven liver cancer models in male mice, we find that psychological stress disrupts catecholamine/β2-adrenergic receptor (ADRB2) signalling, which suppresses the expression of quinolinate phosphoribosyl transferase (QPRT), an enzyme of the kynurenine pathway, in hepatocytes. QPRT loss diverts kynurenine metabolism away from nicotinamide adenine dinucleotide (NAD+) synthesis towards kynurenic acid (KA) accumulation. This shift results in mitochondrial impairment and reduced effector function of liver CD8+ T cells. We confirm that ADRB2/QPRT expression correlates with hepatic NAD+ and KA levels and with CD8+ T cell frequency and function in human liver tissues. Importantly, ADRB2/QPRT overexpression in hepatocytes, or nicotinamide administration, recovers CD8+ T cell function in stressed mice and reduces liver cancer progression. These findings identify a stress-responsive metabolic checkpoint in the liver that links the nervous system to immune surveillance and may be therapeutically targeted in liver cancers. Psychological stress-mediated dysregulation of catecholamine signalling rewires the hepatic kynurenine pathway, which in turn impairs liver CD8+ T cell function and promotes liver cancer progression.
{"title":"Chronic stress drives liver cancer by impairing the hepatic kynurenine pathway and immune surveillance","authors":"Renhui Sun, Deyan Jiao, Wenjing Yuan, Hao Wang, Lingtong Ren, Zhendong Fu, Jiaxuan Zhang, Xuetian Yue, Zhuanchang Wu, Chunyang Li, Huili Hu, Jianping Wang, Lifen Gao, Chunhong Ma, Xiaohong Liang","doi":"10.1038/s42255-025-01430-7","DOIUrl":"10.1038/s42255-025-01430-7","url":null,"abstract":"Psychological stress is increasingly linked to liver disease, but the underlying mechanisms remain unclear. Here we show that chronic stress disrupts a brain–liver circuit that impairs hepatic CD8+ T cell immunity and accelerates liver cancer progression. Using both oncogene-driven and carcinogen-driven liver cancer models in male mice, we find that psychological stress disrupts catecholamine/β2-adrenergic receptor (ADRB2) signalling, which suppresses the expression of quinolinate phosphoribosyl transferase (QPRT), an enzyme of the kynurenine pathway, in hepatocytes. QPRT loss diverts kynurenine metabolism away from nicotinamide adenine dinucleotide (NAD+) synthesis towards kynurenic acid (KA) accumulation. This shift results in mitochondrial impairment and reduced effector function of liver CD8+ T cells. We confirm that ADRB2/QPRT expression correlates with hepatic NAD+ and KA levels and with CD8+ T cell frequency and function in human liver tissues. Importantly, ADRB2/QPRT overexpression in hepatocytes, or nicotinamide administration, recovers CD8+ T cell function in stressed mice and reduces liver cancer progression. These findings identify a stress-responsive metabolic checkpoint in the liver that links the nervous system to immune surveillance and may be therapeutically targeted in liver cancers. Psychological stress-mediated dysregulation of catecholamine signalling rewires the hepatic kynurenine pathway, which in turn impairs liver CD8+ T cell function and promotes liver cancer progression.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"8 1","pages":"196-214"},"PeriodicalIF":20.8,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146003854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-19DOI: 10.1038/s42255-025-01446-z
Gerard Clarke, Lily Keane, John F. Cryan
In this issue of Nature Metabolism, Sun et al. show that the kynurenine pathway of tryptophan metabolism links stress-induced impairment of immune surveillance to liver cancer progression.
{"title":"Hepatic tryptophan metabolism links chronic stress to liver cancer","authors":"Gerard Clarke, Lily Keane, John F. Cryan","doi":"10.1038/s42255-025-01446-z","DOIUrl":"10.1038/s42255-025-01446-z","url":null,"abstract":"In this issue of Nature Metabolism, Sun et al. show that the kynurenine pathway of tryptophan metabolism links stress-induced impairment of immune surveillance to liver cancer progression.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"8 1","pages":"10-11"},"PeriodicalIF":20.8,"publicationDate":"2026-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146003887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-16DOI: 10.1038/s42255-025-01428-1
Kimberly S. Huggler, Kyle M. Flickinger, Matthew H. Forsberg, Carlos A. Mellado Fritz, Gavin R. Chang, Meghan F. McGuire, Christian M. Capitini, Jason R. Cantor
Hexokinase (HK) catalyses the phosphorylation of glucose to glucose 6-phosphate, marking the first step of glucose metabolism. Most cancer cells co-express two homologous HK isoforms, HK1 and HK2, which can each bind the outer mitochondrial membrane (OMM). CRISPR screens performed across hundreds of cancer cell lines indicate that both isoforms are dispensable for growth in conventional culture media. By contrast, HK2 deletion impaired cell growth in human plasma-like medium. Here we show that this conditional HK2 dependence can be traced to the subcellular distribution of HK1. Notably, OMM-detached (cytosolic) rather than OMM-docked HK supports cell growth and aerobic glycolysis (the Warburg effect), an enigmatic phenotype of most proliferating cells. We show that under conditions promoting increased translocation of HK1 to the OMM, HK2 is required for cytosolic HK activity to sustain this phenotype, thereby driving sufficient glycolytic ATP production. Our results reveal a basis for conditional HK2 essentiality and suggest that demand for compartmentalized ATP synthesis explains why cells engage in aerobic glycolysis. Hexokinase detachment from the outer mitochondrial membrane is shown to support aerobic glycolysis in cancer cells. Differential localization of the HK1 isoform to the outer mitochondrial membrane, compared to the HK2 isoform, explains the conditional essentiality of HK2 in cancer cells cultured in physiologic media.
{"title":"Hexokinase detachment from mitochondria drives the Warburg effect to support compartmentalized ATP production","authors":"Kimberly S. Huggler, Kyle M. Flickinger, Matthew H. Forsberg, Carlos A. Mellado Fritz, Gavin R. Chang, Meghan F. McGuire, Christian M. Capitini, Jason R. Cantor","doi":"10.1038/s42255-025-01428-1","DOIUrl":"10.1038/s42255-025-01428-1","url":null,"abstract":"Hexokinase (HK) catalyses the phosphorylation of glucose to glucose 6-phosphate, marking the first step of glucose metabolism. Most cancer cells co-express two homologous HK isoforms, HK1 and HK2, which can each bind the outer mitochondrial membrane (OMM). CRISPR screens performed across hundreds of cancer cell lines indicate that both isoforms are dispensable for growth in conventional culture media. By contrast, HK2 deletion impaired cell growth in human plasma-like medium. Here we show that this conditional HK2 dependence can be traced to the subcellular distribution of HK1. Notably, OMM-detached (cytosolic) rather than OMM-docked HK supports cell growth and aerobic glycolysis (the Warburg effect), an enigmatic phenotype of most proliferating cells. We show that under conditions promoting increased translocation of HK1 to the OMM, HK2 is required for cytosolic HK activity to sustain this phenotype, thereby driving sufficient glycolytic ATP production. Our results reveal a basis for conditional HK2 essentiality and suggest that demand for compartmentalized ATP synthesis explains why cells engage in aerobic glycolysis. Hexokinase detachment from the outer mitochondrial membrane is shown to support aerobic glycolysis in cancer cells. Differential localization of the HK1 isoform to the outer mitochondrial membrane, compared to the HK2 isoform, explains the conditional essentiality of HK2 in cancer cells cultured in physiologic media.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"8 1","pages":"215-236"},"PeriodicalIF":20.8,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145990090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-16DOI: 10.1038/s42255-025-01445-0
Rodrigo Fernández-Verdejo, Kaja Falkenhain, José E. Galgani, Eric Ravussin
Adjusting energy expenditure for body composition and visualizing the results are key to understanding the role of energy expenditure in human physiology and disease. Here, we outline specific analysis of covariance modelling and the design of partial residual plots optimized for analysing human energy expenditure data.
{"title":"Standardizing the analysis and visualization of human energy expenditure data","authors":"Rodrigo Fernández-Verdejo, Kaja Falkenhain, José E. Galgani, Eric Ravussin","doi":"10.1038/s42255-025-01445-0","DOIUrl":"10.1038/s42255-025-01445-0","url":null,"abstract":"Adjusting energy expenditure for body composition and visualizing the results are key to understanding the role of energy expenditure in human physiology and disease. Here, we outline specific analysis of covariance modelling and the design of partial residual plots optimized for analysing human energy expenditure data.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"8 2","pages":"279-281"},"PeriodicalIF":20.8,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145986412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-15DOI: 10.1038/s42255-025-01434-3
Pauline Morigny, Michaela Vondrackova, Honglei Ji, Kristyna Brejchova, Monika Krakovkova, Konstantinos Makris, Radka Trubacova, Tuna F. Samanci, Doris Kaltenecker, Su-Ping Ng, Vignesh Karthikaisamy, Sophia E. Chrysostomou, Anna Bidovec, Mariana Ponce-de-Leon, Tanja Krauss, Claudine Seeliger, Olga Prokopchuk, Marc E. Martignoni, Melina Claussnitzer, Hans Hauner, Martina Schweiger, Laure B. Bindels, Mauricio Berriel Diaz, Stephan Herzig, Dominik Lutter, Ondrej Kuda, Maria Rohm
Cachexia is a wasting disorder associated with high morbidity and mortality in patients with cancer. Tumour–host interaction and maladaptive metabolic reprogramming are substantial, yet poorly understood, contributors to cachexia. Here we present a comprehensive overview of the spatio-temporal metabolic reprogramming during cachexia, using integrated metabolomics, RNA sequencing and 13C-glucose tracing data from multiple tissues and tumours of C26 tumour-bearing male mice at different disease stages. We identified one-carbon metabolism as a tissue-overarching pathway characteristic for metabolic wasting in mice and patients and linked to inflammation, glucose hypermetabolism and atrophy in muscle. The same metabolic rewiring also occurred in five additional mouse models, namely Panc02, 8025, ApcMin, LLC and KPP, and a humanised cachexia mouse model. Together, our study provides a molecular framework for understanding metabolic reprogramming and the multi-tissue metabolite-coordinated response during cancer cachexia progression, with one-carbon metabolism as a tissue-overarching mechanism linked to wasting. Multi-omics profiling of diverse cancer cachexia models uncovers a multi-tissue metabolite-coordinated response associated with disease progression and links multi-tissue one-carbon metabolism to wasting.
{"title":"Multi-omics profiling of cachexia-targeted tissues reveals a spatio-temporally coordinated response to cancer","authors":"Pauline Morigny, Michaela Vondrackova, Honglei Ji, Kristyna Brejchova, Monika Krakovkova, Konstantinos Makris, Radka Trubacova, Tuna F. Samanci, Doris Kaltenecker, Su-Ping Ng, Vignesh Karthikaisamy, Sophia E. Chrysostomou, Anna Bidovec, Mariana Ponce-de-Leon, Tanja Krauss, Claudine Seeliger, Olga Prokopchuk, Marc E. Martignoni, Melina Claussnitzer, Hans Hauner, Martina Schweiger, Laure B. Bindels, Mauricio Berriel Diaz, Stephan Herzig, Dominik Lutter, Ondrej Kuda, Maria Rohm","doi":"10.1038/s42255-025-01434-3","DOIUrl":"10.1038/s42255-025-01434-3","url":null,"abstract":"Cachexia is a wasting disorder associated with high morbidity and mortality in patients with cancer. Tumour–host interaction and maladaptive metabolic reprogramming are substantial, yet poorly understood, contributors to cachexia. Here we present a comprehensive overview of the spatio-temporal metabolic reprogramming during cachexia, using integrated metabolomics, RNA sequencing and 13C-glucose tracing data from multiple tissues and tumours of C26 tumour-bearing male mice at different disease stages. We identified one-carbon metabolism as a tissue-overarching pathway characteristic for metabolic wasting in mice and patients and linked to inflammation, glucose hypermetabolism and atrophy in muscle. The same metabolic rewiring also occurred in five additional mouse models, namely Panc02, 8025, ApcMin, LLC and KPP, and a humanised cachexia mouse model. Together, our study provides a molecular framework for understanding metabolic reprogramming and the multi-tissue metabolite-coordinated response during cancer cachexia progression, with one-carbon metabolism as a tissue-overarching mechanism linked to wasting. Multi-omics profiling of diverse cancer cachexia models uncovers a multi-tissue metabolite-coordinated response associated with disease progression and links multi-tissue one-carbon metabolism to wasting.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"8 1","pages":"237-259"},"PeriodicalIF":20.8,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s42255-025-01434-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145968780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-15DOI: 10.1038/s42255-025-01421-8
Stefan Christen, Karine Redeuil, Laurence Goulet, Maria-Pilar Giner, Isabelle Breton, Riccardo Rota, Adrien Frézal, Atiye Nazari, Pieter Van den Abbeele, Jean-Philippe Godin, Sophie Nutten, Bernard Cuenoud
Nicotinamide adenine dinucleotide (NAD(H)) and its phosphorylated form NADP(H) are vitamin B3-derived redox cofactors essential for numerous metabolic reactions and protein modifications. Various health conditions are associated with disturbances in NAD+ homeostasis. To restore NAD+ levels, the main biosynthetic pathways have been targeted, with nicotinamide (Nam), nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) being the most prominent boosters. However, while many preclinical studies have examined the effects of these precursors, a direct comparison in humans is lacking, and recent rodent research suggests that the NAD+-boosting effects of NR and NMN may depend on their microbial conversion to nicotinic acid (NA), a mechanism not yet confirmed in humans. Here we show in a randomized, open-label, placebo-controlled study in 65 healthy participants that 14 days of supplementation with NR and NMN, but not Nam, comparably increases circulatory NAD+ concentrations in healthy adults. Unlike the chronic effect, only Nam acutely and transiently affects the whole-blood NAD+ metabolome. Using ex vivo fermentation with human microbiota, we identify that NR and NMN give rise to NA and specifically enhance microbial growth and metabolism. We further demonstrate ex vivo in whole blood that NA is a potent NAD+ booster, while NMN, NR and Nam are not. Ultimately, we propose a gut-dependent model for the modes of action of the three NAD+ precursors with NR and NMN elevating circulatory NAD+ via the Preiss–Handler pathway, while rapidly absorbed Nam acutely affects NAD+ levels via the salvage pathway. Overall, these results indicate a dual effect of NR and NMN and their microbially produced metabolite NA: a sustained increase in systemic NAD+ levels and a potent modulator of gut health. ClinicalTrials.gov identifier: NCT05517122 . A comparison of the effects of different NAD+ boosters is lacking. This clinical study compares the efficacy of the NAD+ boosters NR, NMN and Nam in increasing circulating NAD+ levels and analyses their effects on gut microbial metabolism.
{"title":"The differential impact of three different NAD+ boosters on circulatory NAD and microbial metabolism in humans","authors":"Stefan Christen, Karine Redeuil, Laurence Goulet, Maria-Pilar Giner, Isabelle Breton, Riccardo Rota, Adrien Frézal, Atiye Nazari, Pieter Van den Abbeele, Jean-Philippe Godin, Sophie Nutten, Bernard Cuenoud","doi":"10.1038/s42255-025-01421-8","DOIUrl":"10.1038/s42255-025-01421-8","url":null,"abstract":"Nicotinamide adenine dinucleotide (NAD(H)) and its phosphorylated form NADP(H) are vitamin B3-derived redox cofactors essential for numerous metabolic reactions and protein modifications. Various health conditions are associated with disturbances in NAD+ homeostasis. To restore NAD+ levels, the main biosynthetic pathways have been targeted, with nicotinamide (Nam), nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) being the most prominent boosters. However, while many preclinical studies have examined the effects of these precursors, a direct comparison in humans is lacking, and recent rodent research suggests that the NAD+-boosting effects of NR and NMN may depend on their microbial conversion to nicotinic acid (NA), a mechanism not yet confirmed in humans. Here we show in a randomized, open-label, placebo-controlled study in 65 healthy participants that 14 days of supplementation with NR and NMN, but not Nam, comparably increases circulatory NAD+ concentrations in healthy adults. Unlike the chronic effect, only Nam acutely and transiently affects the whole-blood NAD+ metabolome. Using ex vivo fermentation with human microbiota, we identify that NR and NMN give rise to NA and specifically enhance microbial growth and metabolism. We further demonstrate ex vivo in whole blood that NA is a potent NAD+ booster, while NMN, NR and Nam are not. Ultimately, we propose a gut-dependent model for the modes of action of the three NAD+ precursors with NR and NMN elevating circulatory NAD+ via the Preiss–Handler pathway, while rapidly absorbed Nam acutely affects NAD+ levels via the salvage pathway. Overall, these results indicate a dual effect of NR and NMN and their microbially produced metabolite NA: a sustained increase in systemic NAD+ levels and a potent modulator of gut health. ClinicalTrials.gov identifier: NCT05517122 . A comparison of the effects of different NAD+ boosters is lacking. This clinical study compares the efficacy of the NAD+ boosters NR, NMN and Nam in increasing circulating NAD+ levels and analyses their effects on gut microbial metabolism.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"8 1","pages":"62-73"},"PeriodicalIF":20.8,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s42255-025-01421-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145968775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-15DOI: 10.1038/s42255-025-01438-z
Youngjae Jo, Narendra R. Joshi, Karthikeyani Chellappa
Christen et al. present the first comparisons between vitamin B3 and two derivatives that are widely used in humans, showing that the vitamin B3 derivatives rely on microbiome-generated nicotinic acid to synthesize NAD+ and stimulate gut microbial activity.
{"title":"The microbiome at the centre of NAD+ supplementation","authors":"Youngjae Jo, Narendra R. Joshi, Karthikeyani Chellappa","doi":"10.1038/s42255-025-01438-z","DOIUrl":"10.1038/s42255-025-01438-z","url":null,"abstract":"Christen et al. present the first comparisons between vitamin B3 and two derivatives that are widely used in humans, showing that the vitamin B3 derivatives rely on microbiome-generated nicotinic acid to synthesize NAD+ and stimulate gut microbial activity.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"8 1","pages":"4-5"},"PeriodicalIF":20.8,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145986413","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-15DOI: 10.1038/s42255-025-01440-5
Hui Ming, Miao Yin, Qun-Ying Lei
Cachexia is a wasting disorder characterized by progressive metabolic dysregulation. A new study demonstrates using systematic multi-omics analyses that activation of one-carbon metabolism potentially contributes to energy wasting in cachexia, providing in-depth understanding of cachexia in terms of metabolic rewiring.
{"title":"Spatio-temporal metabolic alterations in cachexia","authors":"Hui Ming, Miao Yin, Qun-Ying Lei","doi":"10.1038/s42255-025-01440-5","DOIUrl":"10.1038/s42255-025-01440-5","url":null,"abstract":"Cachexia is a wasting disorder characterized by progressive metabolic dysregulation. A new study demonstrates using systematic multi-omics analyses that activation of one-carbon metabolism potentially contributes to energy wasting in cachexia, providing in-depth understanding of cachexia in terms of metabolic rewiring.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"8 1","pages":"12-13"},"PeriodicalIF":20.8,"publicationDate":"2026-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145990064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-13DOI: 10.1038/s42255-025-01423-6
In pancreatic islets, α-cells secrete glucagon in response to hypoglycaemia. We report that neighbouring δ-cells regulate this process via a negative feedback loop. Hypoglycaemia enhances this intercellular crosstalk, resulting in impaired glucagon response and systemic counter-regulation. Targeting this feedback circuit between α- and δ-cells may help to prevent recurrent iatrogenic hypoglycaemia.
{"title":"Enhanced crosstalk between α- and δ-cells promotes recurrent hypoglycaemia","authors":"","doi":"10.1038/s42255-025-01423-6","DOIUrl":"10.1038/s42255-025-01423-6","url":null,"abstract":"In pancreatic islets, α-cells secrete glucagon in response to hypoglycaemia. We report that neighbouring δ-cells regulate this process via a negative feedback loop. Hypoglycaemia enhances this intercellular crosstalk, resulting in impaired glucagon response and systemic counter-regulation. Targeting this feedback circuit between α- and δ-cells may help to prevent recurrent iatrogenic hypoglycaemia.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"8 1","pages":"14-15"},"PeriodicalIF":20.8,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145961373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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