Life metabolism最新文献_第5页

Abnormal adipose tissue-derived microbes drive metabolic disorder and exacerbate postnatal growth retardation in piglet. 源自脂肪组织的异常微生物会导致代谢紊乱，并加剧仔猪出生后的生长迟缓。

Life metabolism Pub Date : 2024-01-17 eCollection Date: 2024-04-01 DOI: 10.1093/lifemeta/load052

Tongxing Song, Ming Qi, Yucheng Zhu, Nan Wang, Zhibo Liu, Na Li, Jiacheng Yang, Yanxu Han, Jing Wang, Shiyu Tao, Zhuqing Ren, Yulong Yin, Jinshui Zheng, Bie Tan

{"title":"Abnormal adipose tissue-derived microbes drive metabolic disorder and exacerbate postnatal growth retardation in piglet.","authors":"Tongxing Song, Ming Qi, Yucheng Zhu, Nan Wang, Zhibo Liu, Na Li, Jiacheng Yang, Yanxu Han, Jing Wang, Shiyu Tao, Zhuqing Ren, Yulong Yin, Jinshui Zheng, Bie Tan","doi":"10.1093/lifemeta/load052","DOIUrl":"10.1093/lifemeta/load052","url":null,"abstract":"Postnatal growth retardation (PGR) frequently occurs during early postnatal development of piglets and induces high mortality. To date, the mechanism of PGR remains poorly understood. Adipose tissue-derived microbes have been documented to be associated with several disorders of metabolism and body growth. However, the connection between microbial disturbance of adipose tissue and pig PGR remains unclear. Here, we investigated piglets with PGR and found that the adipose tissue of PGR piglets was characterized by metabolism impairment, adipose abnormality, and specific enrichment of culturable bacteria from Proteobacteria. Gavage of Sphingomonas paucimobilis, a species of Sphingomonas genus from the alphaproteobacteria, induced PGR in piglets. Moreover, this bacterium could also lead to metabolic disorders and susceptibility to acute stress, resulting in weight loss in mice. Mechanistically, multi-omics analysis indicated the changes in lipid metabolism as a response of adipose tissue to abnormal microbial composition. Further experimental tests proved that one of the altered lipids phosphatidylethanolamines could rescue the metabolism disorder and growth retardation, thereby suppressing the amount of Sphingomonas in the adipose tissue. Together, these results highlight that the microbe-host crosstalk may regulate the metabolic function of adipose tissue in response to PGR.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"3 2","pages":"load052"},"PeriodicalIF":0.0,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11749387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

IDH1 mutation inhibits differentiation of astrocytes and glioma cells with low OGDH expression by disturbing α-ketoglutarate-related metabolism and epigenetic modification IDH1 基因突变通过干扰α-酮戊二酸相关代谢和表观遗传修饰，抑制了 OGDH 低表达的星形胶质细胞和胶质瘤细胞的分化

Life metabolism Pub Date : 2024-01-15 DOI: 10.1093/lifemeta/loae002

Yuanlin Zhao, Ying Yang, Risheng Yang, Chao Sun, Xing Gao, Xiwen Gu, Yuan Yuan, Yating Nie, Shenhui Xu, Ruili Han, Lijun Zhang, Jing Li, P. Hu, Yingmei Wang, Huangtao Chen, Xiangmei Cao, Jing Wu, Zhe Wang, Yu Gu, Jing Ye

{"title":"IDH1 mutation inhibits differentiation of astrocytes and glioma cells with low OGDH expression by disturbing α-ketoglutarate-related metabolism and epigenetic modification","authors":"Yuanlin Zhao, Ying Yang, Risheng Yang, Chao Sun, Xing Gao, Xiwen Gu, Yuan Yuan, Yating Nie, Shenhui Xu, Ruili Han, Lijun Zhang, Jing Li, P. Hu, Yingmei Wang, Huangtao Chen, Xiangmei Cao, Jing Wu, Zhe Wang, Yu Gu, Jing Ye","doi":"10.1093/lifemeta/loae002","DOIUrl":"https://doi.org/10.1093/lifemeta/loae002","url":null,"abstract":"\u0000 Isocitrate dehydrogenase (IDH) mutations frequently occurr in lower-grade gliomas and secondary glioblastomas. Mutant IDHs exhibit a gain-of-function activity, leading to the production of D-2-hydroxyglutarate (D-2HG) by reducing α-ketoglutarate (α-KG), a central player in metabolism and epigenetic modifications. However, the role of α-KG homeostasis in IDH-mutated gliomagenesis remains elusive. In this study, we found that low expression of oxoglutarate dehydrogenase (OGDH) is a common feature in IDH-mutated gliomas, as well as in astrocytes. This low expression of OGDH results in the accumulation of α-KG and promotes astrocyte maturation. However, IDH1 mutation significantly reduces α-KG levels, and increases glutaminolysis and DNA/histone methylation in astrocytes. These metabolic and epigenetic alterations inhibit astrocyte maturation, and lead to cortical dysplasia in mice. Moreover, our results also indicated that reduced OGDH expression can promote the differentiation of glioma cells, while IDH1 mutations impeded the differentiation of glioma cells with low OGDH by reducing the accumulation of α-K and increasing glutaminolysis. Finally, we found that L-glutamine increased α-KG levels and augmented the differentiation-promoting effects of AGI5198, an IDH1-mutant inhibitor, in IDH1-mutant glioma cells. Collectively, this study reveals that low OGDH expression is a crucial metabolic characteristic of IDH-mutant gliomas, providing a potential strategy for the treatment of IDH-mutant gliomas by targeting α-KG homeostasis.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"28 15","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139528755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Antibody switch AIDed by pyruvate 丙酮酸有助于抗体转换

Life metabolism Pub Date : 2024-01-05 DOI: 10.1093/lifemeta/loae001

Haoming Luan, Tiffany Horng

引用次数: 0

Hepatic TRPC3 loss contributes to chronic alcohol consumption-induced hepatic steatosis and liver injury in mice. 肝脏 TRPC3 的缺失是慢性饮酒诱发小鼠肝脏脂肪变性和肝损伤的原因之一。

Life metabolism Pub Date : 2023-12-18 eCollection Date: 2024-02-01 DOI: 10.1093/lifemeta/load050

Qinchao Ding, Rui Guo, Liuyi Hao, Qing Song, Ai Fu, Shanglei Lai, Tiantian Xu, Hui Zhuge, Kaixin Chang, Yanli Chen, Haibin Wei, Daxi Ren, Zhaoli Sun, Zhenyuan Song, Xiaobing Dou, Songtao Li

{"title":"Hepatic TRPC3 loss contributes to chronic alcohol consumption-induced hepatic steatosis and liver injury in mice.","authors":"Qinchao Ding, Rui Guo, Liuyi Hao, Qing Song, Ai Fu, Shanglei Lai, Tiantian Xu, Hui Zhuge, Kaixin Chang, Yanli Chen, Haibin Wei, Daxi Ren, Zhaoli Sun, Zhenyuan Song, Xiaobing Dou, Songtao Li","doi":"10.1093/lifemeta/load050","DOIUrl":"10.1093/lifemeta/load050","url":null,"abstract":"Emerging evidence discloses the involvement of calcium channel protein in the pathological process of liver diseases. Transient receptor potential cation channel subfamily C member 3 (TRPC3), a ubiquitously expressed non-selective cation channel protein, controls proliferation, inflammation, and immune response via operating calcium influx in various organs. However, our understanding on the biofunction of hepatic TRPC3 is still limited. The present study aims to clarify the role and potential mechanism(s) of TRPC3 in alcohol-associated liver disease (ALD). We recently found that TRPC3 expression plays an important role in the disease process of ALD. Alcohol exposure led to a significant reduction of hepatic TRPC3 in patients with alcohol-related hepatitis (AH) and ALD models. Antioxidants (N-acetylcysteine and mitoquinone) intervention improved alcohol-induced suppression of TRPC3 via a miR-339-5p-involved mechanism. TRPC3 loss robustly aggravated the alcohol-induced hepatic steatosis and liver injury in mouse liver; this was associated with the suppression of Ca2+/calmodulin-dependent protein kinase kinase 2 (CAMKK2)/AMP-activated protein kinase (AMPK) and dysregulation of genes related to lipid metabolism. TRPC3 loss also enhanced hepatic inflammation and early fibrosis-like change in mice. Replenishing hepatic TRPC3 effectively reversed chronic alcohol-induced detrimental alterations in ALD mice. Briefly, chronic alcohol exposure-induced TRPC3 reduction contributes to the pathological development of ALD via suppression of the CAMKK2/AMPK pathway. Oxidative stress-stimulated miR-339-5p upregulation contributes to alcohol-reduced TRPC3. TRPC3 is the requisite and a potential target to defend alcohol consumption-caused ALD.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"3 1","pages":"load050"},"PeriodicalIF":0.0,"publicationDate":"2023-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11749259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Join the club: YIPF3 and YIPF4 act as Golgiphagy receptors 加入俱乐部YIPF3和YIPF4作为Golgiphagy受体发挥作用

Life metabolism Pub Date : 2023-12-09 DOI: 10.1093/lifemeta/load049

Xiaoli Ma, Hong Zhang

引用次数: 0

Hyperoxidized PRDX3 as a specific ferroptosis marker. 过氧化的 PRDX3 是一种特异性铁变态反应标记。

Life metabolism Pub Date : 2023-12-01 Epub Date: 2023-11-18 DOI: 10.1093/lifemeta/load042

Yuelong Yan, Boyi Gan

引用次数: 0

Metabolic restraining of epigenetic modifications promotes cardiomyocyte proliferation 代谢抑制表观遗传修饰促进心肌细胞增殖

Life metabolism Pub Date : 2023-12-01 DOI: 10.1093/lifemeta/load047

Xiuxiu Liu, Bin Zhou

引用次数: 0

A metabolic signaling role for arginine in liver cancer 精氨酸在肝癌中的代谢信号作用

Life metabolism Pub Date : 2023-11-27 DOI: 10.1093/lifemeta/load046

David Sokolov, Lucas B Sullivan

引用次数: 0

Regulation of hepatic lipid metabolism by intestine epithelium-derived exosomes 肠上皮源性外泌体对肝脏脂质代谢的调控

Life metabolism Pub Date : 2023-11-21 DOI: 10.1093/lifemeta/load044

Tiange Feng, Yuan Liang, Lijun Sun, Lu Feng, Jiajie Min, Michael W Mulholland, Yue Yin, Weizhen Zhang

{"title":"Regulation of hepatic lipid metabolism by intestine epithelium-derived exosomes","authors":"Tiange Feng, Yuan Liang, Lijun Sun, Lu Feng, Jiajie Min, Michael W Mulholland, Yue Yin, Weizhen Zhang","doi":"10.1093/lifemeta/load044","DOIUrl":"https://doi.org/10.1093/lifemeta/load044","url":null,"abstract":"The “gut-liver axis” is critical for the control of hepatic lipid homeostasis, where the intestine affects the liver through multiple pathways such as nutrient uptake, gastrointestinal hormone release, and gut microbiota homeostasis. Whether intestine-originated exosomes mediate the gut’s influence on liver steatosis remains unknown. Here we aimed to determine whether intestinal epithelium-derived exosomes (intExos) contribute to the regulation of hepatic lipid metabolism. We found that mouse intExos could be taken up by hepatic cells. Mice fed high-fat diet (HFD) received intExos showed strong resistance to liver steatosis. MicroRNA sequencing of intExos indicated the correlation between miR-21a-5p/miR-145a-5p and hepatic lipid metabolism. Both liver overexpression of miR-21a-5p and intExos containing miR-21a-5p alleviated hepatic steatosis in mice fed with HFD. Mechanistically, miR-21a-5p suppressed the expression of Ccl1 (C-C motif chemokine ligand 1) in macrophages, as well as lipid transport genes Cd36 (cluster of differentiation 36) and Fabp7 (fatty acid binding protein 7) in hepatocytes. Liver-specific inhibition of miR-145a-5p significantly reduced hepatic lipid accumulation in mice fed with HFD through negatively regulating the expression of Btg1 (BTG anti-proliferation factor 1), leading to an increase of stearoyl-CoA desaturase-1 and lipogenesis.Our study demonstrates that intExos regulate hepatic lipid metabolism and NAFLD (non-alcoholic fatty liver disease) progression via miR-21a-5p and miR-145a-5p pathways, providing novel mediators for the gut-liver crosstalk and potential targets for regulating hepatic lipid metabolism.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"63 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139250806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Single-nucleus RNA sequencing reveals heterogeneity among multiple white adipose tissue depots 单核 RNA 测序揭示了多种白色脂肪组织贮备的异质性

Life metabolism Pub Date : 2023-11-21 DOI: 10.1093/lifemeta/load045

Limin Xie, Wanyu Hu, Haowei Zhang, Yujin Ding, Qin Zeng, Xiyan Liao, Dandan Wang, Wanqin Xie, Xiaoyan Hui, Tuo Deng

{"title":"Single-nucleus RNA sequencing reveals heterogeneity among multiple white adipose tissue depots","authors":"Limin Xie, Wanyu Hu, Haowei Zhang, Yujin Ding, Qin Zeng, Xiyan Liao, Dandan Wang, Wanqin Xie, Xiaoyan Hui, Tuo Deng","doi":"10.1093/lifemeta/load045","DOIUrl":"https://doi.org/10.1093/lifemeta/load045","url":null,"abstract":"Regardless of its anatomical site, adipose tissue shares a common energy-storage role but exhibits distinctive properties. Exploring the cellular and molecular heterogeneity of white adipose tissue (WAT) is crucial for comprehending its function and properties. However, existing single-nucleus RNA sequencing (snRNA-seq) studies of adipose tissue heterogeneity have examined only one or two depots. In this study, we employed snRNA-seq to test five representative depots including inguinal, epididymal, mesenteric, perirenal, and pericardial adipose tissues in mice under physiological conditions. By analyzing the contents of main cell categories and gene profiles of various depots, we identified their distinctive physiological properties. Immune cells and fibro-adipogenic progenitor cells (FAPs) showed dramatic differences among WAT depots, while adipocytes seemed to be conserved. The heightened presence of regulatory macrophages and B cells in pericardial adipose tissues implied their potential contribution to the preservation of coronary vascular function. Moreover, the selective aggregation of pericytes within mesenteric adipose tissue was likely associated with the maintenance of intestinal barrier homeostasis. Using a combination of RNA sequencing and snRNA-seq analysis, the major subpopulations of FAPs derived from these depots determined the site characteristics of FAPs to a certain extent. Our work establishes a systematic and reliable foundation for investigating the heterogeneity of WAT depots and elucidating the unique roles these depots play in coordinating the function of adjacent organs.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"242 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139252397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0