Life metabolism最新文献_第5页

Myokines: metabolic regulation in obesity and type 2 diabetes 肌动蛋白：肥胖症和 2 型糖尿病的代谢调节机制

Life metabolism Pub Date : 2024-03-02 DOI: 10.1093/lifemeta/loae006

Zhi-Tian Chen, Zhi-Xuan Weng, Jiandie D. Lin, Zhuo-Xian Meng

{"title":"Myokines: metabolic regulation in obesity and type 2 diabetes","authors":"Zhi-Tian Chen, Zhi-Xuan Weng, Jiandie D. Lin, Zhuo-Xian Meng","doi":"10.1093/lifemeta/loae006","DOIUrl":"https://doi.org/10.1093/lifemeta/loae006","url":null,"abstract":"\u0000 Skeletal muscle plays a vital role in the regulation of systemic metabolism, partly through its secretion of endocrine factors which are collectively known as myokines. Altered myokine levels are associated with metabolic diseases, such as type 2 diabetes (T2D). The significance of interorgan crosstalk, particularly through myokines, has emerged as a fundamental aspect of nutrient and energy homeostasis. However, a comprehensive understanding of myokine biology in the setting of obesity and T2D remains a major challenge. In this review, we discuss the regulation and biological functions of key myokines that have been extensively studied during the past two decades, namely interleukin 6 (IL-6), irisin, myostatin (MSTN), growth differentiation factor 11 (GDF11), fibroblast growth factor 21 (FGF21), apelin, brain-derived neurotrophic factor (BDNF), meteorin-like (Metrnl), secreted protein acidic and rich in cysteine (SPARC), β-aminoisobutyric acid (BAIBA), Musclin, and Dickkopf-3 (Dkk3). Related to these, we detail the role of exercise in myokine expression and secretion together with their contributions to metabolic physiology and disease. Despite significant advancements in myokine research, many myokines remain challenging to measure accurately and investigate thoroughly. Hence, new research techniques and detection methods should be developed and rigorously tested. Therefore, developing a comprehensive perspective on myokine biology is crucial, as this will likely offer new insights into the pathophysiological mechanisms underlying obesity and T2D and may reveal novel targets for therapeutic interventions.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"13 24","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140082259","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

Lipidomic remodeling during mammalian preimplantation embryonic development 哺乳动物植入前胚胎发育过程中的脂质体重塑

Life metabolism Pub Date : 2024-02-28 DOI: 10.1093/lifemeta/loae005

Qingran Kong, Shaorong Gao

引用次数: 0

Size matters: the biochemical logic of ligand type in endocrine crosstalk. 大小很重要：内分泌串联中配体类型的生化逻辑。

Life metabolism Pub Date : 2024-02-01 Epub Date: 2023-12-08 DOI: 10.1093/lifemeta/load048

Jameel Barkat Lone, Jonathan Z Long, Katrin J Svensson

引用次数: 0

The secretory function of adipose tissues in metabolic regulation 脂肪组织在新陈代谢调节中的分泌功能

Life metabolism Pub Date : 2024-01-20 DOI: 10.1093/lifemeta/loae003

Yang Liu, S. Qian, Yang Tang, Qi-Qun Tang

{"title":"The secretory function of adipose tissues in metabolic regulation","authors":"Yang Liu, S. Qian, Yang Tang, Qi-Qun Tang","doi":"10.1093/lifemeta/loae003","DOIUrl":"https://doi.org/10.1093/lifemeta/loae003","url":null,"abstract":"\u0000 In addition to their pivotal roles in energy storage and expenditure, adipose tissues play a crucial part in the secretion of bioactive molecules, including peptides, lipids, metabolites, and extracellular vesicles, in response to physiological stimulation and metabolic stress. These secretory factors, through autocrine and paracrine mechanisms, regulate various processes within adipose tissues. These processes include adipogenesis, glucose and lipid metabolism, inflammation, and adaptive thermogenesis, all of which are essential for the maintenance of the balance and functionality of the adipose tissue micro-environment. A subset of these adipose-derived secretory factors can enter the circulation and target the distant tissues to regulate appetite, cognitive function, energy expenditure, insulin secretion and sensitivity, gluconeogenesis, cardiovascular remodeling, and exercise capacity. In this review, we highlight the role of adipose-derived secretory factors and their signaling pathways in modulating metabolic homeostasis. Furthermore, we delve into the alterations in both the content and secretion processes of these factors under various physiological and pathological conditions, shedding light on potential pharmacological treatment strategies for related diseases.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"6 11","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139524215","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

Long-chain acyl-CoA synthetase regulates systemic lipid homeostasis via glycosylation-dependent lipoprotein production 长链酰基-CoA 合成酶通过糖基化依赖性脂蛋白生成调节全身脂质平衡

Life metabolism Pub Date : 2024-01-18 DOI: 10.1093/lifemeta/loae004

Jie Li, Yue Dong, Tianxing Zhou, He Tian, Xiahe Huang, Yong Q Zhang, Yingchun Wang, S. Lam, G. Shui

{"title":"Long-chain acyl-CoA synthetase regulates systemic lipid homeostasis via glycosylation-dependent lipoprotein production","authors":"Jie Li, Yue Dong, Tianxing Zhou, He Tian, Xiahe Huang, Yong Q Zhang, Yingchun Wang, S. Lam, G. Shui","doi":"10.1093/lifemeta/loae004","DOIUrl":"https://doi.org/10.1093/lifemeta/loae004","url":null,"abstract":"\u0000 Interorgan lipid transport is crucial for organism development and the maintenance of physiological function. Here, we demonstrate that Drosophila long-chain acyl-CoA synthetase (dAcsl), which catalyzes the conversion of fatty acids into acyl-coenzyme As (acyl-CoAs), plays a critical role in regulating systemic lipid homeostasis. dAcsl deficiency in the fat body leads to the ectopic accumulation of neutral lipids in the gut, along with significantly reduced lipoprotein contents in both the fat body and hemolymph. The aberrant phenotypes were rescued by fat body-specific overexpression of apolipophorin. A multi-omics investigation comprising lipidomics, metabolomics, and proteomics in conjunction with genetic screening revealed that glycosylation processes were suppressed in dAcsl knockdowns. Overexpression of CG9035, human ortholog of which is implicated in the congenital disorder of glycosylation, ameliorated gut lipid accumulation in Drosophila. Aberrant lipoprotein glycosylation led to accelerated proteasome-related degradation and induced ER stress in dAcsl knockdown flies, impairing lipoprotein release into the circulation which compromised interorgan lipid transport between the fat body and the gut. Inhibition of ubiquitin-proteasome-dependent degradation alleviated the phenotype of gut ectopic fat accumulation in dAcsl knockdowns. Finally, we verified that ACSL4, the human homolog of dAcsl, also regulated lipoprotein levels in HepG2 cells, indicating that the role of dAcsl in modulating lipoprotein secretion and systemic lipid homeostasis is possibly conserved in humans.","PeriodicalId":74074,"journal":{"name":"Life metabolism","volume":"109 23","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139614794","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

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