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The mTORC1 complex in pre-osteoblasts regulates whole-body energy metabolism independently of osteocalcin

Bone Research 2021年第1期9卷 109-125页

作者： Pawanrat Tangseefa sally K.Martin Peck Yin Chin james Breen Chui Yan Mah Paul A.Baldock Gary A.Wittert Amanda j.Page Christopher G.Proud stephen Fitter Andrew C.W.Zannettino Adelaide Medical school Faculty of Health and Medical ScienceUniversity of AdelaideAdelaide5005 SAAustralia Cancer Program Precision Medicine ThemeSouth Australian Health and Medical Research InstituteAdelaide5000 SAAustralia Research Centre for Reproductive Health School of Paediatrics and Reproductive HealthUniversity of AdelaideAdelaide5005 SAAustralia Computational&systems Biology program Precision Medicine ThemeSouth Australian Health and Medical Research InstituteAdelaide5000 SAAustralia robinson Research Institute University of AdelaideAdelaideSA 5005Australia Bioinformatics Hub University of AdelaideAdelaideSA 5005Australia Freemasons Foundation Centre for Men’s Health University of AdelaideAdelaide5005 SAAustralia skeletal Metabolism Group Garvan Institute of Medical ResearchSydney2010 NSWAustralia Nutrition Diabetes&Metabolism ProgramLifelong Health ThemeSouth Australian Health and Medical Research InstituteAdelaide5000 SAAustralia school of Biological sciences University of AdelaideAdelaide5005 SAAustralia Central Adelaide Local Health Network AdelaideSAAustralia

Overnutrition causes hyperactivation of mTORC1-dependent negative feedback loops leading to the downregulation of insulin signaling and development of insulin *** osteoblasts(OBs),insulin signaling plays a crucial role in the control of systemic glucose *** utilized mice with conditional deletion of Rptor to investigate how the loss of mTORC1 function in OB affects glucose metabolism under normal and overnutrition dietary *** to the controls,chow-fed Rptorob−/−mice had substantially less fat mass and exhibited adipocyte ***,upon feeding with high-fat diet,mice with pre-and post-natal deletion of Rptor in OBs were protected from diet-induced obesity and exhibited improved glucose metabolism with lower fasting glucose and insulin levels,increased glucose tolerance and insulin *** leanness and resistance to weight gain was not attributable to changes in food intake,physical activity or lipid absorption but instead was due to increased energy expenditure and greater whole-body substrate ***-seq revealed an increase in glycolysis and skeletal insulin signaling pathways,which correlated with the potentiation of insulin signaling and increased insulin-dependent glucose uptake in Rptorknockout ***,these findings point to a critical role for the mTORC1 complex in the skeletal regulation of wholebody glucose metabolism and the skeletal development of insulin resistance.

关键词： metabolism mTORC1 homeostasis

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新研究确定了与肝病和脂肪代谢有关的肝细胞突变

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中西医结合肝病杂志 2021年第11期31卷 1011-1011页

作者： stanley W. K. Ng Foad j. Rouhani simon F. Brunner Natalia Brzozowska Federico Abascal Luiza Moore Lia Chappell Daniel Leongamornlert Aleksandra Ivovic Philip robinson Timothy Butler Mathijs A. sanders Nicholas Williams Tim H. H. Coorens jon Teague Keiran Raine Adam P. Butler Yvette Hooks Beverley Wilson Natalie Birtchnell Michael R. stratton Iñigo Martincorena Raheleh Rahbari Peter j. Campbell Foad j. Rouhani & Huw Naylor sarah j. Aitken & Matthew Hoare sarah j. Aitken & susan E. Davies sarah j. Aitken Ming Yang Efterpi Nikitopoulou Christian Frezza Matthew Hoare Cancer Genome Project Wellcome Sanger Institute Hinxton UK Department of Hematology Erasmus University Medical Center Rotterdam The Netherlands stem Cell Institute University of Cambridge Cambridge UK Department of surgery Addenbrooke’s Hospital Cambridge UK CRUK Cambridge Institute Cambridge UK Department of Pathology Addenbrooke’s Hospital Cambridge UK MRC Toxicology Unit University of Cambridge Cambridge UK MRC Cancer Unit University of Cambridge Cambridge UK Department of Medicine University of Cambridge Addenbrooke’s Hospital Cambridge UK

一项来自英国韦尔科姆基金会桑格研究所和剑桥大学等研究机构的研究人员的新研究分析了来自34例患者肝脏样本的1590个基因组,包括健康对照、酒精相关肝病和非酒精性脂肪肝疾病患者的肝脏样本,结果发现ACVR2A、TNRC6B、NEAT1、FOXO1和GP... 详细信息

一项来自英国韦尔科姆基金会桑格研究所和剑桥大学等研究机构的研究人员的新研究分析了来自34例患者肝脏样本的1590个基因组,包括健康对照、酒精相关肝病和非酒精性脂肪肝疾病患者的肝脏样本,结果发现ACVR2A、TNRC6B、NEAT1、FOXO1和GPAM 五个基因在肝病患者的肝细胞中发生了突变,过程如图a所示。而其中的FOXO1、CIDEB、GPAM三个基因是对肝细胞如何代谢脂肪和对胰岛素作出反应有直接影响的基因。

关键词： FOXO1 肝病患者细胞突变肝细胞脂肪代谢胰岛素 GPA 剑桥大学

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Challenges and solutions in patient treatment strategies for stage Ⅱ colon cancer

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Gastroenterology Report 2019年第3期7卷 151-161,I0001页

作者： susan Fotheringham Guy A.Mozolowski Eleanor M.A.Murray David j.Kerr Oxford Cancer Biomarkers Limited The Magdalen CentreThe Oxford Science ParkRobert Robinson AvenueOxfordOX44GAUK The Medical school The University of SheffieldBeech Hill RoadSheffieldS102RXUK Nuffield Department of Clinical Laboratory sciences Level 4 Academic BlockJohn Radcliffe HospitalHeadingtonOxfordOX39DUUK

Colorectal cancer remains one of the most common cancers worldwide and,despite improvements in treatment options for late-stage metastatic cancer,there are still questions surrounding how best to treat early-stage disease *** recent advances have been made in the staging of cancer and improving the risk assessment of strategies for patient treatment.A number of high-risk features have been proposed that may help to stratify stage Ⅱ cancer patients into groups that will truly benefit from adjuvant *** tests are becoming available to measure these biomarkers,utilizing both currently available and novel *** review will describe the challenges in treatment decisions for early-stage colon cancer and how personalized medicine can assist clinicians in making the best treatment choices for patients with stage Ⅱ colon cancer in particular.

关键词： Colorectal cancer treatment strategy challenge

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妊娠中期母亲血清甲胎蛋白水平变化与产后婴儿猝死综合征之间的关系

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世界核心医学期刊文摘（儿科学分册） 2005年第3期1卷 8-8页

作者： smith G.C.s. Wood A.M. Pell j.P. 刘健 Department of Obstetrics Cambridge University Rosie Maternity Hospital Robinson Way Cambridge CB2 2QQ United Kingdom

背景:不明原因的死产和婴儿猝死综合征(sIDs)都有一些相同的特点,在妊娠中期,母亲血清甲胎蛋白水平增高,表明胎盘功能障碍,也是胎儿不明原因死产的一个重要提示。母亲血清甲胎蛋白水平增高是否也可以预示sIDs的发生,尚不清楚。方法:作... 详细信息

背景:不明原因的死产和婴儿猝死综合征(sIDs)都有一些相同的特点,在妊娠中期,母亲血清甲胎蛋白水平增高,表明胎盘功能障碍,也是胎儿不明原因死产的一个重要提示。母亲血清甲胎蛋白水平增高是否也可以预示sIDs的发生,尚不清楚。方法:作者通过对苏格兰西部妇产医院提供的资料,包括产前信息、围生期胎儿死亡情况以及婴儿出生和死亡等情况进行评估。

关键词：血清甲胎蛋白婴儿猝死综合征妊娠中期围生期水平变化胎盘功能负相关

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