Cell metabolism最新文献_第8页

Microbial-host isozyme: A novel target in "drug the bug" strategies for diabetes. 微生物宿主同工酶：糖尿病“药虫”策略中的一个新靶点。

Cell metabolism Pub Date : 2023-10-03 DOI: 10.1016/j.cmet.2023.09.008

Guojun Wu, Naisi Zhao, Liping Zhao

引用次数: 0

She didn't start the fire: Mammary duct epithelial cells suppress adipocyte thermogenesis. 她没有引起火灾：乳腺管上皮细胞抑制脂肪细胞的产热。

Cell metabolism Pub Date : 2023-10-03 DOI: 10.1016/j.cmet.2023.09.007

David Merrick

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Targeting Pathogenic Lafora Bodies in Lafora Disease Using an Antibody-Enzyme Fusion. 使用抗体-酶融合靶向拉福拉病中的致病性拉福拉体。

Cell metabolism Pub Date : 2019-10-01 Epub Date: 2019-07-25 DOI: 10.1016/j.cmet.2019.07.002

M Kathryn Brewer, Annette Uittenbogaard, Grant L Austin, Dyann M Segvich, Anna DePaoli-Roach, Peter J Roach, John J McCarthy, Zoe R Simmons, Jason A Brandon, Zhengqiu Zhou, Jill Zeller, Lyndsay E A Young, Ramon C Sun, James R Pauly, Nadine M Aziz, Bradley L Hodges, Tracy R McKnight, Dustin D Armstrong, Matthew S Gentry

{"title":"Targeting Pathogenic Lafora Bodies in Lafora Disease Using an Antibody-Enzyme Fusion.","authors":"M Kathryn Brewer, Annette Uittenbogaard, Grant L Austin, Dyann M Segvich, Anna DePaoli-Roach, Peter J Roach, John J McCarthy, Zoe R Simmons, Jason A Brandon, Zhengqiu Zhou, Jill Zeller, Lyndsay E A Young, Ramon C Sun, James R Pauly, Nadine M Aziz, Bradley L Hodges, Tracy R McKnight, Dustin D Armstrong, Matthew S Gentry","doi":"10.1016/j.cmet.2019.07.002","DOIUrl":"https://doi.org/10.1016/j.cmet.2019.07.002","url":null,"abstract":"Lafora disease (LD) is a fatal childhood epilepsy caused by recessive mutations in either the EPM2A or EPM2B gene. A hallmark of LD is the intracellular accumulation of insoluble polysaccharide deposits known as Lafora bodies (LBs) in the brain and other tissues. In LD mouse models, genetic reduction of glycogen synthesis eliminates LB formation and rescues the neurological phenotype. Therefore, LBs have become a therapeutic target for ameliorating LD. Herein, we demonstrate that human pancreatic α-amylase degrades LBs. We fused this amylase to a cell-penetrating antibody fragment, and this antibody-enzyme fusion (VAL-0417) degrades LBs in vitro and dramatically reduces LB loads in vivo in Epm2a-/- mice. Using metabolomics and multivariate analysis, we demonstrate that VAL-0417 treatment of Epm2a-/- mice reverses the metabolic phenotype to a wild-type profile. VAL-0417 is a promising drug for the treatment of LD and a putative precision therapy platform for intractable epilepsy.","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":"30 4","pages":"689-705.e6"},"PeriodicalIF":0.0,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.cmet.2019.07.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41223576","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

Thermoneutral Housing Accelerates Metabolic Inflammation to Potentiate Atherosclerosis but Not Insulin Resistance. 中温住房会加速代谢炎症，从而加剧动脉粥样硬化，但不会加剧胰岛素抵抗。

Cell metabolism Pub Date : 2016-01-12 Epub Date: 2015-11-05 DOI: 10.1016/j.cmet.2015.10.003

Xiao Yu Tian, Kirthana Ganeshan, Cynthia Hong, Khoa D Nguyen, Yifu Qiu, Jason Kim, Rajendra K Tangirala, Peter Tontonoz, Peter Tonotonoz, Ajay Chawla

{"title":"Thermoneutral Housing Accelerates Metabolic Inflammation to Potentiate Atherosclerosis but Not Insulin Resistance.","authors":"Xiao Yu Tian, Kirthana Ganeshan, Cynthia Hong, Khoa D Nguyen, Yifu Qiu, Jason Kim, Rajendra K Tangirala, Peter Tontonoz, Peter Tonotonoz, Ajay Chawla","doi":"10.1016/j.cmet.2015.10.003","DOIUrl":"10.1016/j.cmet.2015.10.003","url":null,"abstract":"Chronic, low-grade inflammation triggered by excess intake of dietary lipids has been proposed to contribute to the pathogenesis of metabolic disorders, such as obesity, insulin resistance, type 2 diabetes, and atherosclerosis. Although considerable evidence supports a causal association between inflammation and metabolic diseases, most tests of this link have been performed in cold-stressed mice that are housed below their thermoneutral zone. We report here that thermoneutral housing of mice has a profound effect on the development of metabolic inflammation, insulin resistance, and atherosclerosis. Mice housed at thermoneutrality develop metabolic inflammation in adipose tissue and in the vasculature at an accelerated rate. Unexpectedly, this increased inflammatory response contributes to the progression of atherosclerosis but not insulin resistance. These findings not only suggest that metabolic inflammation can be uncoupled from obesity-associated insulin resistance, but also point to how thermal stress might limit our ability to faithfully model human diseases in mice. ","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":"23 1","pages":"165-78"},"PeriodicalIF":0.0,"publicationDate":"2016-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4715491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141285662","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

Impairment of central leptin-mediated PI3K signaling manifested as hepatic steatosis independent of hyperphagia and obesity. 中枢瘦素介导的 PI3K 信号转导受损表现为肝脂肪变性，与多食和肥胖无关。

Cell metabolism Pub Date : 2011-12-07 DOI: 10.1016/j.cmet.2011.11.001

James P Warne, Farzad Alemi, Alison S Reed, Jillian M Varonin, Helen Chan, Merisa L Piper, Mark E Mullin, Martin G Myers, Carlos U Corvera, Allison W Xu

{"title":"Impairment of central leptin-mediated PI3K signaling manifested as hepatic steatosis independent of hyperphagia and obesity.","authors":"James P Warne, Farzad Alemi, Alison S Reed, Jillian M Varonin, Helen Chan, Merisa L Piper, Mark E Mullin, Martin G Myers, Carlos U Corvera, Allison W Xu","doi":"10.1016/j.cmet.2011.11.001","DOIUrl":"https://doi.org/10.1016/j.cmet.2011.11.001","url":null,"abstract":"Hepatic steatosis is generally thought to develop via peripheral mechanisms associated with obesity. We show that chronic central infusion of leptin suppresses hepatic lipogenic gene expression and reduces triglyceride content via stimulation of hepatic sympathetic activity. This leptin function is independent of feeding and body weight but requires phosphatidylinositol 3-kinase (PI3K) signaling. Attenuation of leptin-induced PI3K signaling, brought about by transgenic expression of phosphatase and tensin homolog (PTEN) in leptin receptor neurons, leads to decreased hepatic sympathetic tone and increased triglyceride levels without affecting adiposity or hepatic insulin signaling. Central leptin's effects on hepatic norepinephrine levels and triglyceride content are blunted in these mutant mice. Simultaneous downregulation of PI3K and signal transducer and activator of transcription-3 (Stat3) in leptin receptor neurons does not exacerbate obesity but causes more severe hepatic steatosis. Together, our results indicate that central cellular leptin resistance in PI3K signaling manifests as hepatic steatosis without causing obesity.","PeriodicalId":93927,"journal":{"name":"Cell metabolism","volume":"14 6","pages":"791-803"},"PeriodicalIF":0.0,"publicationDate":"2011-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3240844/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141452357","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