Life metabolism最新文献_第3页

Immuno-electron microscopy localizes Caenorhabditis elegans vitellogenins along the classic exocytosis route 免疫电子显微镜确定秀丽隐杆线虫卵黄原蛋白的经典外渗路线

Life metabolism Pub Date : 2024-06-13 DOI: 10.1093/lifemeta/loae025

Chao Zhai, Nan Zhang, Xixia Li, Xue-Ke Tan, Fei Sun, Meng-Qiu Dong

{"title":"Immuno-electron microscopy localizes Caenorhabditis elegans vitellogenins along the classic exocytosis route","authors":"Chao Zhai, Nan Zhang, Xixia Li, Xue-Ke Tan, Fei Sun, Meng-Qiu Dong","doi":"10.1093/lifemeta/loae025","DOIUrl":"https://doi.org/10.1093/lifemeta/loae025","url":null,"abstract":"\u0000 Vitellogenins (VITs) are the most abundant proteins in adult hermaphrodite Caenorhabditis elegans. VITs are synthesized in the intestine, secreted to the pseudocoelom, matured into yolk proteins, and finally deposited in oocytes as nutrients for progeny developme nt. How VITs are secreted out of the intestine remains unclear. Using immuno-electron microscopy (immuno-EM), we localize intestinal VITs along an exocytic pathway consisting of the rough endoplasmic reticulum (ER), the Golgi, and the lipid bilayer-bounded VIT vesicles (VVs). This suggests that the classic exocytotic pathway mediates the secretion of VITs from the intestine to the pseudocoelom. We also show that pseudocoelomic yolk patches (PYPs) are membrane-less and amorphous. The different VITs/yolk proteins are packed as a mixture into the above structures. The size of VVs can vary with the VIT levels and the age of the worm. On adult day 2 (AD 2), intestinal VVs (~200 nm in diameter) are smaller than gonadal yolk organelles (YOs, ~500 nm in diameter). VVs, PYPs, and YOs share a uniform medium electron density by conventional EM. The morphological profiles documented in this study serve as a reference for future studies of VITs/yolk proteins.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"3 8","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141346708","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

Protecting liver health with microbial-derived succinylated bile acids 用微生物提取的琥珀酰化胆汁酸保护肝脏健康

Life metabolism Pub Date : 2024-06-13 DOI: 10.1093/lifemeta/loae023

H. Demagny, A. Perino, Kristina Schoonjans

引用次数: 0

Cholesin, a new hormone bridges intestinal cholesterol absorption and hepatic synthesis 胆固醇素--一种连接肠道胆固醇吸收和肝脏合成的新激素

Life metabolism Pub Date : 2024-06-07 DOI: 10.1093/lifemeta/loae024

Peter U Amadi, Da-wei Zhang

引用次数: 0

Downregulation of RhoA/ROCK1/YAP/F-actin causing decreased aortic smooth muscle cell stiffness promotes aortic dissection formation RhoA/ROCK1/YAP/F-actin 的下调导致主动脉平滑肌细胞硬度下降，从而促进主动脉夹层的形成

Life metabolism Pub Date : 2024-06-03 DOI: 10.1093/lifemeta/loae022

Wei Zhang, Mengxiao Wang, Enci Wang, Wei Lu, Zengxia Li, Yuchong Zhang, Gaofei Hu, Qi Zhang, Wenxin Shan, Yongjun Dang, Zhe Zhao, Lemin Zheng, Weiguo Fu, Lixin Wang

引用次数: 0

The energetics of cellular life transitions. 细胞生命转换的能量学。

Life metabolism Pub Date : 2024-06-01 Epub Date: 2023-12-27 DOI: 10.1093/lifemeta/load051

Anna S Monzel, Michael Levin, Martin Picard

引用次数: 0

Spatial multi-omics characterizes GPR35-relevant lipid metabolism signatures across liver zonation in MASLD. 空间多组学研究了MASLD中与gpr35相关的脂质代谢特征。

Life metabolism Pub Date : 2024-05-31 eCollection Date: 2024-12-01 DOI: 10.1093/lifemeta/loae021

Wuxiyar Otkur, Yiran Zhang, Yirong Li, Wenjun Bao, Tingze Feng, Bo Wu, Yaolu Ma, Jing Shi, Li Wang, Shaojun Pei, Wen Wang, Jixia Wang, Yaopeng Zhao, Yanfang Liu, Xiuling Li, Tian Xia, Fangjun Wang, Di Chen, Xinmiao Liang, Hai-Long Piao

{"title":"Spatial multi-omics characterizes GPR35-relevant lipid metabolism signatures across liver zonation in MASLD.","authors":"Wuxiyar Otkur, Yiran Zhang, Yirong Li, Wenjun Bao, Tingze Feng, Bo Wu, Yaolu Ma, Jing Shi, Li Wang, Shaojun Pei, Wen Wang, Jixia Wang, Yaopeng Zhao, Yanfang Liu, Xiuling Li, Tian Xia, Fangjun Wang, Di Chen, Xinmiao Liang, Hai-Long Piao","doi":"10.1093/lifemeta/loae021","DOIUrl":"10.1093/lifemeta/loae021","url":null,"abstract":"Metabolic dysfunction-associated steatotic liver disease (MASLD) is a metabolic disease that can progress to metabolic dysfunction-associated steatohepatitis (MASH), cirrhosis, and cancer. The zonal distribution of biomolecules in the liver is implicated in mediating the disease progression. Recently, G-protein-coupled receptor 35 (GPR35) has been highlighted to play a role in MASLD, but the precise mechanism is not fully understood, particularly, in a liver-zonal manner. Here, we aimed to identify spatially distributed specific genes and metabolites in different liver zonation that are regulated by GPR35 in MASLD, by combining lipid metabolomics, spatial transcriptomics (ST), and spatial metabolomics (SM). We found that GPR35 influenced lipid accumulation, inflammatory and metabolism-related factors in specific regions, notably affecting the anti-inflammation factor ELF4 (E74 like E-twenty six (ETS) transcription factor 4), lipid homeostasis key factor CIDEA (cell death-inducing DNA fragmentation factor alpha (DFFA)-like effector A), and the injury response-related genes SAA1/2/3 (serum amyloid A1/2/3), thereby impacting MASLD progression. Furthermore, SM elucidated specific metabolite distributions across different liver regions, such as C10H11N4O7P (3',5'-cyclic inosine monophosphate (3',5'-IMP)) for the central vein, and this metabolite significantly decreased in the liver zones of GPR35-deficient mice during MASLD progression. Taken together, GPR35 regulates hepatocyte damage repair, controls inflammation, and prevents MASLD progression by influencing phospholipid homeostasis and gene expression in a zonal manner.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"3 6","pages":"loae021"},"PeriodicalIF":0.0,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11748505/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054440","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

Genome-wide CRISPR screens identify PTPN21 and WDR26 as modulators of the mitochondrial stress-induced ISR. 全基因组CRISPR筛选鉴定PTPN21和WDR26是线粒体应激诱导的ISR的调节剂。

Life metabolism Pub Date : 2024-05-28 eCollection Date: 2024-08-01 DOI: 10.1093/lifemeta/loae020

Wen Li, Mingyue Dong, Kaiyu Gao, Jialiang Guan, Ying Liu

引用次数: 0

TET2: the fat controller of leptin. TET2：瘦素的脂肪控制者。

Life metabolism Pub Date : 2024-05-24 eCollection Date: 2024-08-01 DOI: 10.1093/lifemeta/loae019

Callen C Goldsmith, Garron T Dodd

引用次数: 0

Fatty acid oxidation-induced HIF-1α activation facilitates hepatic urate synthesis through upregulating NT5C2 and XDH 脂肪酸氧化诱导的 HIF-1α 激活通过上调 NT5C2 和 XDH 促进肝脏尿酸盐合成

Life metabolism Pub Date : 2024-05-17 DOI: 10.1093/lifemeta/loae018

Ningning Liang, Xuan Yuan, Lili Zhang, Xia Shen, Shanshan Zhong, Luxiao Li, Rui Li, Xiaodong Xu, Xin Chen, Chunzhao Yin, Shuyuan Guo, Jing Ge, Mingjiang Zhu, Yongzhen Tao, Shiting Chen, Yongbing Qian, Nicola Dalbeth, Tony R. Merriman, R. Terkeltaub, Changgui Li, Qiang Xia, Huiyong Yin

{"title":"Fatty acid oxidation-induced HIF-1α activation facilitates hepatic urate synthesis through upregulating NT5C2 and XDH","authors":"Ningning Liang, Xuan Yuan, Lili Zhang, Xia Shen, Shanshan Zhong, Luxiao Li, Rui Li, Xiaodong Xu, Xin Chen, Chunzhao Yin, Shuyuan Guo, Jing Ge, Mingjiang Zhu, Yongzhen Tao, Shiting Chen, Yongbing Qian, Nicola Dalbeth, Tony R. Merriman, R. Terkeltaub, Changgui Li, Qiang Xia, Huiyong Yin","doi":"10.1093/lifemeta/loae018","DOIUrl":"https://doi.org/10.1093/lifemeta/loae018","url":null,"abstract":"\u0000 Dyslipidemia affects approximately half of all people with gout, and prior Mendelian randomization analysis suggested a causal role for elevated triglycerides in hyperuricemia (HU), but the underlying mechanisms remain elusive. We hypothesize that dyslipidemia promotes hepatic urate biosynthesis in HU and gout and fatty acid (FA) oxidation (FAO) drives this process. Here we developed a targeted metabolomics to quantify major metabolites in purine metabolic pathway in the sera of a human cohort with HU, gout, and normaluricemic controls. We found that the levels of major purine metabolites and multiple FAs were significantly elevated in HU and gout, compared to normouricemic controls, whereas hypoxathine showed opposite trend. Furthermore, the levels of multiple serum FAs were positively correlated with urate, xanthine, and inosine but negatively with hypoxanthine, which was also observed in a murine model of high-fat diet-induced HU. Using a stable isotope labeled metabolic flux assay, we discovered that exogenous hypoxanthine plays a key role in urate synthesis. Moreover, FAO-induced hypoxia-inducible factor 1 alpha (HIF-1α) activation upregulated 5’-nucleotidase II (NT5C2) and xanthine dehydrogenase (XDH) levels to facilitate hypoxanthine uptake from blood to liver and activation of urate biosynthesis. Our findings was further supported by data in human hepatocytes and 50 paired serum and liver tissues from liver transplant donors.Together, this study uncovers a mechanism by which FAO promotes hepatic urate synthesis by activating HIF-1α-NT5C2/XDH pathways, directly linking lipid metabolism to HU.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"2 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140963036","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

Hypoxia makes EZH2 inhibitor not easy—advances of crosstalk between HIF and EZH2 缺氧使 EZH2 抑制剂难以发挥作用--HIF 与 EZH2 之间的相互影响

Life metabolism Pub Date : 2024-05-06 DOI: 10.1093/lifemeta/loae017

Zhanya Huang, Yuanjun Tang, Jianlin Zhang, Jiaqi Huang, Rui Cheng, Yunyun Guo, Celina G Kleer, Yuqing Wang, Lixiang Xue

引用次数: 0