Nature metabolism最新文献_第2页

Subcutaneous depth-selective spectral imaging with mμSORS enables noninvasive glucose monitoring

IF 20.8 1区医学

Nature metabolism Pub Date : 2025-02-05 DOI: 10.1038/s42255-025-01217-w

Yifei Zhang, Lili Zhang, Long Wang, Shuai Shao, Bei Tao, Chunrui Hu, Yufei Chen, Yue Shen, Xianbiao Zhang, Shijia Pan, Hua Cao, Ming Sun, Jia Shi, Chunhong Jiang, Minghui Chen, Lin Zhou, Guang Ning, Chang Chen, Weiqing Wang

{"title":"Subcutaneous depth-selective spectral imaging with mμSORS enables noninvasive glucose monitoring","authors":"Yifei Zhang, Lili Zhang, Long Wang, Shuai Shao, Bei Tao, Chunrui Hu, Yufei Chen, Yue Shen, Xianbiao Zhang, Shijia Pan, Hua Cao, Ming Sun, Jia Shi, Chunhong Jiang, Minghui Chen, Lin Zhou, Guang Ning, Chang Chen, Weiqing Wang","doi":"10.1038/s42255-025-01217-w","DOIUrl":"https://doi.org/10.1038/s42255-025-01217-w","url":null,"abstract":"Noninvasive blood glucose monitoring offers substantial advantages for patients, but current technologies are often not sufficiently accurate for clinical applications or require personalized calibration. Here we report multiple μ-spatially offset Raman spectroscopy, which captures Raman signals at varying skin depths, and show that it accurately detects blood glucose levels in humans. In 35 individuals with or without type 2 diabetes, we first determine the optimal depth for glucose detection to be at or below the capillary-rich dermal–epidermal junction, where we observe a strong correlation between specific Raman bands and venous plasma glucose concentrations. In a second study, comprising 230 participants, we then improve accuracy of our regression model to reach a mean absolute relative difference of 14.6%, without personalized calibration, whereby 99.4% of calculated glucose values fall into clinically acceptable zones of the consensus error grid (zones A and B). These findings highlight the ability and robustness of multiple μ-spatially offset Raman spectroscopy for noninvasive blood glucose measurement in a clinical setting.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"40 1","pages":""},"PeriodicalIF":20.8,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143125107","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}

引用次数: 0

Maternal exercise prevents metabolic disorders in offspring mice through SERPINA3C

IF 20.8 1区医学

Nature metabolism Pub Date : 2025-01-31 DOI: 10.1038/s42255-024-01213-6

Yang Li, Ruo-Ying Li, Jie-Ying Zhu, Min Chen, Wang-Jing Mu, Hong-Yang Luo, Shan Li, Lin-Jing Yan, Meng-Ting Yin, Xin Li, Hu-Min Chen, Liang Guo

{"title":"Maternal exercise prevents metabolic disorders in offspring mice through SERPINA3C","authors":"Yang Li, Ruo-Ying Li, Jie-Ying Zhu, Min Chen, Wang-Jing Mu, Hong-Yang Luo, Shan Li, Lin-Jing Yan, Meng-Ting Yin, Xin Li, Hu-Min Chen, Liang Guo","doi":"10.1038/s42255-024-01213-6","DOIUrl":"https://doi.org/10.1038/s42255-024-01213-6","url":null,"abstract":"Maternal exercise can improve the metabolic health of the offspring. However, the molecular mechanisms underlying the beneficial effects of maternal exercise on the offspring remain unclear. Here, we show that maternal exercise during pregnancy alleviates high-fat diet (HFD)-induced adipose inflammation and glucose intolerance in offspring mice, accompanied by upregulation of the adipokine serine protease inhibitor A3C (SERPINA3C) both in maternal adipose tissues and the fetal circulation. Adipose SERPINA3C knockdown impairs, but its overexpression in dams mimics, maternal exercise-mediated metabolic benefits in HFD-fed offspring. Maternal SERPINA3C is transported into the fetal circulation and promotes Krüppel-like factor 4 (Klf4) gene promoter demethylation in fetal preadipocytes to increase KLF4 expression, which inhibits adipose inflammation in HFD-fed offspring mice. The SERPINA3C–cathepsin G–integrin β1 axis activates phosphatidylinositol 3-kinase signalling in preadipocytes. This promotes nuclear translocation of the p110β subunit to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3) in the nucleus. O-linked β-N-acetylglucosamine (O-GlcNAc) transferase then binds to PIP3 to promote ten–eleven translocation methylcytosine dioxygenase 1 (TET1) O-GlcNAcylation, thereby enhancing TET1 activity to facilitate Klf4 gene promoter demethylation. These results provide mechanistic insights into maternal exercise-mediated improvement of offspring metabolism.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"23 1","pages":""},"PeriodicalIF":20.8,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143071533","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}

引用次数: 0

SERPINA3C as a mediator of metabolic health in offspring

IF 20.8 1区医学

Nature metabolism Pub Date : 2025-01-31 DOI: 10.1038/s42255-024-01209-2

Bianca E. Suur, Emma Börgeson

引用次数: 0

Epigenetic modification increases skeletal muscle resilience to metabolic stress

IF 20.8 1区医学

Nature metabolism Pub Date : 2025-01-27 DOI: 10.1038/s42255-024-01211-8

引用次数: 0

Kdm2a inhibition in skeletal muscle improves metabolic flexibility in obesity

IF 20.8 1区医学

Nature metabolism Pub Date : 2025-01-27 DOI: 10.1038/s42255-024-01210-9

Yuhan Wang, Hao Xie, Qianrui Liu, Na Wang, Xi Luo, Fei Sun, Jinghan Zhu, Ruihan Dong, Yi Wang, Jia Gao, Zhichao Gao, Teng Huang, Xin Liu, Qilin Yu, Ting Wang, Yang Li, Danni Song, Shiwei Liu, Shu Zhang, Hao Yin, Wen Kong, Cong-Yi Wang

{"title":"Kdm2a inhibition in skeletal muscle improves metabolic flexibility in obesity","authors":"Yuhan Wang, Hao Xie, Qianrui Liu, Na Wang, Xi Luo, Fei Sun, Jinghan Zhu, Ruihan Dong, Yi Wang, Jia Gao, Zhichao Gao, Teng Huang, Xin Liu, Qilin Yu, Ting Wang, Yang Li, Danni Song, Shiwei Liu, Shu Zhang, Hao Yin, Wen Kong, Cong-Yi Wang","doi":"10.1038/s42255-024-01210-9","DOIUrl":"https://doi.org/10.1038/s42255-024-01210-9","url":null,"abstract":"Skeletal muscle is a critical organ in maintaining homoeostasis against metabolic stress, and histone post-translational modifications are pivotal in those processes. However, the intricate nature of histone methylation in skeletal muscle and its impact on metabolic homoeostasis have yet to be elucidated. Here, we report that mitochondria-rich slow-twitch myofibers are characterized by significantly higher levels of H3K36me2 along with repressed expression of Kdm2a, an enzyme that specifically catalyses H3K36me2 demethylation. Deletion or inhibition of Kdm2a shifts fuel use from glucose under cold challenge to lipids under obese conditions by increasing the proportion of mitochondria-rich slow-twitch myofibers. This protects mice against cold insults and high-fat-diet-induced obesity and insulin resistance. Mechanistically, Kdm2a deficiency leads to a marked increase in H3K36me2 levels, which then promotes the recruitment of Mrg15 to the Esrrg locus to process its precursor messenger RNA splicing, thereby reshaping skeletal muscle metabolic profiles to induce slow-twitch myofiber transition. Collectively, our data support the role of Kdm2a as a viable target against metabolic stress.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"4 1","pages":""},"PeriodicalIF":20.8,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143044162","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}

引用次数: 0

Astrocyte-to-neuron H2O2 signalling supports long-term memory formation in Drosophila and is impaired in an Alzheimer’s disease model

IF 20.8 1区医学

Nature metabolism Pub Date : 2025-01-24 DOI: 10.1038/s42255-024-01189-3

Yasmine Rabah, Jean-Paul Berwick, Nisrine Sagar, Laure Pasquer, Pierre-Yves Plaçais, Thomas Preat

{"title":"Astrocyte-to-neuron H2O2 signalling supports long-term memory formation in Drosophila and is impaired in an Alzheimer’s disease model","authors":"Yasmine Rabah, Jean-Paul Berwick, Nisrine Sagar, Laure Pasquer, Pierre-Yves Plaçais, Thomas Preat","doi":"10.1038/s42255-024-01189-3","DOIUrl":"https://doi.org/10.1038/s42255-024-01189-3","url":null,"abstract":"Astrocytes help protect neurons from potential damage caused by reactive oxygen species (ROS). While ROS can also exert beneficial effects, it remains unknown how neuronal ROS signalling is activated during memory formation, and whether astrocytes play a role in this process. Here we discover an astrocyte-to-neuron H2O2 signalling cascade in Drosophila that is essential for long-term memory formation. Stimulation of astrocytes by acetylcholine induces an increase in intracellular calcium ions, which triggers the generation of extracellular superoxide (O2•–) by astrocytic NADPH oxidase. Astrocyte-secreted superoxide dismutase 3 (Sod3) converts O2•– to hydrogen peroxide (H2O2), which is imported into neurons of the olfactory memory centre, the mushroom body, as revealed by in vivo H2O2 imaging. Notably, Sod3 activity requires copper ions, which are supplied by neuronal amyloid precursor protein. We also find that human amyloid-β peptide, implicated in Alzheimer’s disease, inhibits the nAChRα7 astrocytic cholinergic receptor and impairs memory formation by preventing H2O2 synthesis. These findings may have important implications for understanding the aetiology of Alzheimer’s disease.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"38 1","pages":""},"PeriodicalIF":20.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143026712","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}

引用次数: 0

Memory with a little H2O2 help from astrocyte friends

IF 20.8 1区医学

Nature metabolism Pub Date : 2025-01-24 DOI: 10.1038/s42255-024-01212-7

Katerina Papanikolopoulou, Eirini-Maria Georganta, Efthimios MC Skoulakis

引用次数: 0

Author Correction: Intestinal TM6SF2 protects against metabolic dysfunction-associated steatohepatitis through the gut–liver axis 作者更正：肠道TM6SF2通过肠-肝轴保护代谢功能障碍相关的脂肪性肝炎。

IF 18.9 1区医学

Nature metabolism Pub Date : 2025-01-21 DOI: 10.1038/s42255-025-01215-y

Xiang Zhang, Harry Cheuk-Hay Lau, Suki Ha, Chuanfa Liu, Cong Liang, Hye Won Lee, Queena Wing-Yin Ng, Yi Zhao, Fenfen Ji, Yunfei Zhou, Yasi Pan, Yang Song, Yating Zhang, Jennie Ching Yin Lo, Alvin Ho Kwan Cheung, Jianfeng Wu, Xiaoxing Li, Hongzhi Xu, Chi Chun Wong, Vincent Wai-Sun Wong, Jun Yu

引用次数: 0

Aldolase A: the broker of glycolysis 醛缩酶A：糖酵解的中间人

IF 20.8 1区医学

Nature metabolism Pub Date : 2025-01-20 DOI: 10.1038/s42255-024-01202-9

Luiza Martins Nascentes Melo, Feyza Cansiz, Alpaslan Tasdogan

引用次数: 0

Targeting aldolase A in hepatocellular carcinoma leads to imbalanced glycolysis and energy stress due to uncontrolled FBP accumulation 在肝细胞癌中靶向醛缩酶A会导致不平衡的糖酵解和能量应激，因为不受控制的FBP积累

IF 20.8 1区医学

Nature metabolism Pub Date : 2025-01-20 DOI: 10.1038/s42255-024-01201-w

Marteinn T. Snaebjornsson, Philipp Poeller, Daria Komkova, Florian Röhrig, Lisa Schlicker, Alina M. Winkelkotte, Adriano B. Chaves-Filho, Kamal M. Al-Shami, Carolina Dehesa Caballero, Ioanna Koltsaki, Felix C. E. Vogel, Roberto Carlos Frias-Soler, Ramona Rudalska, Jessica D. Schwarz, Elmar Wolf, Daniel Dauch, Ralf Steuer, Almut Schulze

{"title":"Targeting aldolase A in hepatocellular carcinoma leads to imbalanced glycolysis and energy stress due to uncontrolled FBP accumulation","authors":"Marteinn T. Snaebjornsson, Philipp Poeller, Daria Komkova, Florian Röhrig, Lisa Schlicker, Alina M. Winkelkotte, Adriano B. Chaves-Filho, Kamal M. Al-Shami, Carolina Dehesa Caballero, Ioanna Koltsaki, Felix C. E. Vogel, Roberto Carlos Frias-Soler, Ramona Rudalska, Jessica D. Schwarz, Elmar Wolf, Daniel Dauch, Ralf Steuer, Almut Schulze","doi":"10.1038/s42255-024-01201-w","DOIUrl":"https://doi.org/10.1038/s42255-024-01201-w","url":null,"abstract":"Increased glycolytic flux is a hallmark of cancer; however, an increasing body of evidence indicates that glycolytic ATP production may be dispensable in cancer, as metabolic plasticity allows cancer cells to readily adapt to disruption of glycolysis by increasing ATP production via oxidative phosphorylation. Using functional genomic screening, we show here that liver cancer cells show a unique sensitivity toward aldolase A (ALDOA) depletion. Targeting glycolysis by disrupting the catalytic activity of ALDOA led to severe energy stress and cell cycle arrest in murine and human hepatocellular carcinoma cell lines. With a combination of metabolic flux analysis, metabolomics, stable-isotope tracing and mathematical modelling, we demonstrate that inhibiting ALDOA induced a state of imbalanced glycolysis in which the investment phase outpaced the payoff phase. Targeting ALDOA effectively converted glycolysis from an energy producing into an energy-consuming process. Moreover, we found that depletion of ALDOA extended survival and reduced cancer cell proliferation in an animal model of hepatocellular carcinoma. Thus, our findings indicate that induction of imbalanced glycolysis by targeting ALDOA presents a unique opportunity to overcome the inherent metabolic plasticity of cancer cells.","PeriodicalId":19038,"journal":{"name":"Nature metabolism","volume":"49 1","pages":""},"PeriodicalIF":20.8,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142989920","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}

引用次数: 0