Life metabolism最新文献

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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

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.

低级别胶质瘤和继发性胶质母细胞瘤中经常出现异柠檬酸脱氢酶（IDH）突变。突变的 IDH 具有功能增益活性，可通过减少α-酮戊二酸（α-KG）产生 D-2-羟基戊二酸（D-2HG），而α-KG 是新陈代谢和表观遗传修饰的核心角色。然而，α-KG平衡在IDH突变胶质瘤发生过程中的作用仍然难以捉摸。在这项研究中，我们发现氧戊二酸脱氢酶（OGDH）的低表达是IDH突变胶质瘤以及星形胶质细胞的共同特征。OGDH 的低表达会导致 α-KG 的积累，并促进星形胶质细胞的成熟。然而，IDH1突变会显著降低α-KG水平，并增加星形胶质细胞中的谷氨酰胺溶解和DNA/组蛋白甲基化。这些代谢和表观遗传学改变抑制了星形胶质细胞的成熟，并导致小鼠皮质发育不良。此外，我们的研究结果还表明，OGDH表达的减少可促进胶质瘤细胞的分化，而IDH1突变则通过减少α-K的积累和增加谷氨酰胺的溶解，阻碍了低OGDH胶质瘤细胞的分化。最后，我们发现，L-谷氨酰胺能提高α-KG的水平，并增强IDH1突变抑制剂AGI5198对IDH1突变胶质瘤细胞的分化促进作用。总之，这项研究揭示了低OGDH表达是IDH突变胶质瘤的一个重要代谢特征，为通过靶向α-KG平衡治疗IDH突变胶质瘤提供了一种潜在的策略。

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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

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.

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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

The lack of a reliable and specific marker for ferroptosis has hindered the advancement of treatments related to this cell death mechanism toward clinical application. A recent study published in Molecular Cell has identified hyperoxidized peroxiredoxin 3 (PRDX3) as a promising marker for ferroptosis, opening up new avenues for monitoring and targeting ferroptosis in disease treatment.

由于缺乏可靠而特异的铁中毒标记物，阻碍了与这种细胞死亡机制有关的治疗方法走向临床应用。最近发表在《分子细胞》（Molecular Cell）上的一项研究发现，过氧化过氧还蛋白3（PRDX3）是一种有希望的铁中毒标记物，这为在疾病治疗中监测和靶向铁中毒开辟了新途径。

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

The metabolic state of a cell is closely related to its structure and function in adult mammalian cardiomyocytes. These adult cardiomyocytes primarily use fatty acids as an energy substrate to support heart contraction. Recently, Li and his colleagues reported that inhibiting fatty acid oxidation in cardiomyocytes keeps them in an immature state. This influences epigenomic modifications and ultimately increases the proliferation capacity of the cardiomyocytes.

在成年哺乳动物心肌细胞中，细胞的代谢状态与其结构和功能密切相关。这些成年心肌细胞主要使用脂肪酸作为能量底物来支持心脏收缩。最近，李和他的同事报告说，抑制心肌细胞中的脂肪酸氧化使它们处于不成熟状态。这影响表观基因组修饰，并最终增加心肌细胞的增殖能力。

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

In addition to their canonical roles in biosynthetic pathways, metabolites can be active participants in oncogenic signaling, but our understanding of these signaling mechanisms is incomplete. In a recent article published in Cell, Mossmann and colleagues find a novel signaling role for accumulated arginine in hepatocellular carcinoma (HCC), mediated by the RNA splicing factor and transcriptional modifier RNA-binding protein 39 (RBM39).

除了在生物合成途径中的典型作用外，代谢物还可能是致癌信号转导的积极参与者，但我们对这些信号转导机制的了解还不全面。在最近发表于《细胞》（Cell）的一篇文章中，Mossmann 及其同事发现肝细胞癌（HCC）中积累的精氨酸具有新的信号作用，它由 RNA 剪接因子和转录修饰因子 RNA 结合蛋白 39 (RBM39) 介导。

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

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.

肠肝轴 "对控制肝脏脂质平衡至关重要，肠道通过营养摄取、胃肠激素释放和肠道微生物群平衡等多种途径影响肝脏。肠道源性外泌体是否介导肠道对肝脏脂肪变性的影响仍是未知数。在此，我们旨在确定肠上皮源性外泌体（intExos）是否有助于调节肝脏脂质代谢。我们发现小鼠的肠外泌体可被肝细胞吸收。接受intExos的高脂饮食（HFD）小鼠对肝脏脂肪变性有很强的抵抗力。intExos的微RNA测序表明，miR-21a-5p/miR-145a-5p与肝脏脂质代谢相关。肝脏过量表达miR-21a-5p和含有miR-21a-5p的intExos都能缓解高纤维食物喂养小鼠的肝脂肪变性。从机理上讲，miR-21a-5p抑制了巨噬细胞中Ccl1（C-C motif趋化因子配体1）以及肝细胞中脂质转运基因Cd36（分化簇36）和Fabp7（脂肪酸结合蛋白7）的表达。肝特异性抑制 miR-145a-5p，可通过负向调节 Btg1（BTG 抗增殖因子 1）的表达，导致硬脂酰-CoA 去饱和酶-1 的增加和脂肪生成，从而显著减少高脂饮食喂养小鼠的肝脏脂质积累。我们的研究表明，intExos通过miR-21a-5p和miR-145a-5p途径调控肝脏脂质代谢和NAFLD（非酒精性脂肪肝）的进展，为肠道-肝脏串联提供了新的媒介和调控肝脏脂质代谢的潜在靶点。

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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

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.

无论解剖部位如何，脂肪组织都有一个共同的储能作用，但却表现出与众不同的特性。探索白色脂肪组织（WAT）的细胞和分子异质性对于理解其功能和特性至关重要。然而，现有的关于脂肪组织异质性的单核 RNA 测序（snRNA-seq）研究只考察了一个或两个脂肪库。在本研究中，我们采用 snRNA-seq 技术检测了生理条件下小鼠腹股沟、附睾、肠系膜、肾周和心包等五个代表性脂肪组织。通过分析不同脂肪组织的主要细胞类别和基因谱，我们确定了它们各自不同的生理特性。免疫细胞和纤维-成脂祖细胞（FAPs）在不同的脂肪组织中显示出巨大的差异，而脂肪细胞似乎是一致的。调节性巨噬细胞和 B 细胞在心包脂肪组织中的高度存在意味着它们对冠状动脉血管功能的保护具有潜在的贡献。此外，肠系膜脂肪组织中的周细胞选择性聚集可能与肠屏障稳态的维持有关。利用RNA测序和snRNA-seq分析相结合的方法，从这些储层中提取的FAPs主要亚群在一定程度上确定了FAPs的部位特征。我们的工作为研究 WAT 储库的异质性和阐明这些储库在协调相邻器官功能方面的独特作用奠定了系统而可靠的基础。

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引用次数: 0

Exercise training improves long-term memory in obese mice 运动训练可改善肥胖小鼠的长期记忆力

Life metabolism

Pub Date : 2023-11-15 DOI: 10.1093/lifemeta/load043

O. K. Fuller, Casey L. Egan, Tina L Robinson, Nimna Perera, Heidy K Latchman, Lauren V Terry, Emma D. McLennan, Carolina Chavez, Emma L. Burrows, John W Scott, Robyn M Murphy, H. van Praag, M. Whitham, M. Febbraio

Obesity has been linked to a range of pathologies, including dementia. In contrast, regular physical activity is associated with the prevention or reduced progression of neurodegeneration. Specifically, physical activity can improve memory and spatial cognition, reduce age-related cognitive decline, and preserve brain volume, but the mechanisms are not fully understood. Accordingly, we investigated whether any detrimental effects of high-fat diet (HFD)-induced obesity on cognition, motor behavior, adult hippocampal neurogenesis, and brain-derived neurotrophic factor (BDNF) could be mitigated by voluntary exercise training in male C57Bl/6 mice. HFD-induced impairment of motor function was not reversed by exercise. Importantly, voluntary wheel running improved long-term memory and increased hippocampal neurogenesis, suggesting that regular physical activity may prevent cognitive decline in obesity.

肥胖与包括痴呆症在内的一系列病症有关。相比之下，有规律的体育锻炼与预防或减少神经退行性变的进展有关。具体来说，体育锻炼可以改善记忆力和空间认知能力，减少与年龄相关的认知能力衰退，并保持脑容量，但其机制尚不完全清楚。因此，我们研究了高脂饮食（HFD）诱导的肥胖对认知、运动行为、成年海马神经发生和脑源性神经营养因子（BDNF）的不利影响是否可以通过雄性C57Bl/6小鼠的自愿运动训练来缓解。运动并不能逆转HFD引起的运动功能损伤。重要的是，自愿轮跑可改善长期记忆并增加海马神经发生，这表明经常进行体育锻炼可预防肥胖导致的认知功能下降。

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