Defects in beta cell Ca2+ signalling, glucose metabolism and insulin secretion in a murine model of KATP channel-induced neonatal diabetes mellitus
Author:
Publisher
Springer Science and Business Media LLC
Subject
Endocrinology, Diabetes and Metabolism,Internal Medicine
Link
http://link.springer.com/content/pdf/10.1007/s00125-010-2039-7.pdf
Reference31 articles.
1. Nichols CG (2006) K-ATP channels as molecular sensors of cellular metabolism. Nature 440:470–476
2. Hattersley AT, Ashcroft FM (2005) Activating mutations in Kir6.2 and neonatal diabetes—new clinical syndromes, new scientific insights, and new therapy. Diabetes 54:2503–2513
3. Gloyn AL, Pearson ER, Antcliff JF et al (2004) Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes. N Engl J Med 350:1838–1849
4. Koster JC, Marshall BA, Ensor N, Corbett JA, Nichols CG (2000) Targeted overactivity of beta cell K-ATP channels induces profound neonatal diabetes. Cell 100:645–654
5. Remedi MS, Kurata HT, Scott A et al (2009) Secondary consequences of beta cell inexcitability: identification and prevention in a murine model of K-ATP-induced neonatal diabetes mellitus. Cell Metab 9:140–151
Cited by 32 articles. 订阅此论文施引文献 订阅此论文施引文献，注册后可以免费订阅5篇论文的施引文献，订阅后可以查看论文全部施引文献
1. Atypical KCNQ1/Kv7 channel function in a neonatal diabetes patient: Hypersecretion preceded the failure of pancreatic β-cells;iScience;2024-07
2. Altered glycolysis triggers impaired mitochondrial metabolism and mTORC1 activation in diabetic β-cells;Nature Communications;2022-11-14
3. Genetic Reduction of Glucose Metabolism Preserves Functional β-Cell Mass in KATP-Induced Neonatal Diabetes;Diabetes;2022-03-16
4. SGLT2 inhibitors therapy protects glucotoxicity-induced β-cell failure in a mouse model of human KATP-induced diabetes through mitigation of oxidative and ER stress;PLOS ONE;2022-02-18
5. SGLT2 inhibitors therapy protects glucotoxicity-induced β-cell failure in a mouse model of human KATP-induced diabetes trough mitigation of oxidative and ER stress;2021-09-17
1.学者识别学者识别
2.学术分析学术分析
3.人才评估人才评估
"同舟云学术"是以全球学者为主线，采集、加工和组织学术论文而形成的新型学术文献查询和分析系统，可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容，当前同舟云学术共收录了国内外主流学术期刊6万余种，收集的期刊论文及会议论文总量共计约1.5亿篇，并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询！咨询电话：010-8811{复制后删除}0370
www.globalauthorid.com
TOP
Copyright © 2019-2024 北京同舟云网络信息技术有限公司 京公网安备11010802033243号 京ICP备18003416号-3