• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

mTOR 复合物对 Akt 介导的脂肪细胞对胰岛素反应影响的排队论模型。

Queueing theory model of mTOR complexes' impact on Akt-mediated adipocytes response to insulin.

机构信息

Department of Forensic Medicine, Nicolaus Copernicus University Ludwik Rydygier Collegium Medicum, Bydgoszcz, Poland.

Faculty of Telecommunications, Computer Science and Electrical Engineering, Bydgoszcz University of Science and Technology, Bydgoszcz, Poland.

出版信息

PLoS One. 2022 Dec 27;17(12):e0279573. doi: 10.1371/journal.pone.0279573. eCollection 2022.

DOI:10.1371/journal.pone.0279573
PMID:36574435
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9794039/
Abstract

A queueing theory based model of mTOR complexes impact on Akt-mediated cell response to insulin is presented in this paper. The model includes several aspects including the effect of insulin on the transport of glucose from the blood into the adipocytes with the participation of GLUT4, and the role of the GAPDH enzyme as a regulator of mTORC1 activity. A genetic algorithm was used to optimize the model parameters. It can be observed that mTORC1 activity is related to the amount of GLUT4 involved in glucose transport. The results show the relationship between the amount of GAPDH in the cell and mTORC1 activity. Moreover, obtained results suggest that mTORC1 inhibitors may be an effective agent in the fight against type 2 diabetes. However, these results are based on theoretical knowledge and appropriate experimental tests should be performed before making firm conclusions.

摘要

本文提出了一种基于排队论的 mTOR 复合物对胰岛素介导的细胞反应的影响模型。该模型包括几个方面,包括胰岛素对葡萄糖从血液向脂肪细胞运输的影响,以及 GAPDH 酶作为 mTORC1 活性调节剂的作用。遗传算法被用于优化模型参数。可以观察到,mTORC1 活性与参与葡萄糖运输的 GLUT4 数量有关。结果表明了细胞内 GAPDH 的数量与 mTORC1 活性之间的关系。此外,研究结果表明,mTORC1 抑制剂可能是对抗 2 型糖尿病的有效药物。然而,这些结果是基于理论知识得出的,在得出确定的结论之前,应该进行适当的实验测试。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3e8/9794039/778944180030/pone.0279573.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3e8/9794039/194ea70bbb07/pone.0279573.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3e8/9794039/f473b138d9e6/pone.0279573.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3e8/9794039/00a69af7df4d/pone.0279573.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3e8/9794039/e87313b100ec/pone.0279573.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3e8/9794039/778944180030/pone.0279573.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3e8/9794039/194ea70bbb07/pone.0279573.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3e8/9794039/f473b138d9e6/pone.0279573.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3e8/9794039/00a69af7df4d/pone.0279573.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3e8/9794039/e87313b100ec/pone.0279573.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b3e8/9794039/778944180030/pone.0279573.g005.jpg

相似文献

1
Queueing theory model of mTOR complexes' impact on Akt-mediated adipocytes response to insulin.mTOR 复合物对 Akt 介导的脂肪细胞对胰岛素反应影响的排队论模型。
PLoS One. 2022 Dec 27;17(12):e0279573. doi: 10.1371/journal.pone.0279573. eCollection 2022.
2
Insulin signaling in type 2 diabetes: experimental and modeling analyses reveal mechanisms of insulin resistance in human adipocytes.2 型糖尿病中的胰岛素信号转导:实验和建模分析揭示了人脂肪细胞胰岛素抵抗的机制。
J Biol Chem. 2013 Apr 5;288(14):9867-9880. doi: 10.1074/jbc.M112.432062. Epub 2013 Feb 11.
3
Cardiac PI3K-Akt impairs insulin-stimulated glucose uptake independent of mTORC1 and GLUT4 translocation.心脏中的磷脂酰肌醇-3激酶-蛋白激酶B(PI3K-Akt)会损害胰岛素刺激的葡萄糖摄取,且与哺乳动物雷帕霉素靶蛋白复合体1(mTORC1)和葡萄糖转运蛋白4(GLUT4)转位无关。
Mol Endocrinol. 2013 Jan;27(1):172-84. doi: 10.1210/me.2012-1210. Epub 2012 Nov 30.
4
Activation of the mammalian target of rapamycin pathway acutely inhibits insulin signaling to Akt and glucose transport in 3T3-L1 and human adipocytes.雷帕霉素哺乳动物靶点通路的激活会急性抑制3T3-L1细胞和人脂肪细胞中胰岛素向Akt的信号传导以及葡萄糖转运。
Endocrinology. 2005 Mar;146(3):1328-37. doi: 10.1210/en.2004-0777. Epub 2004 Dec 2.
5
Systems-wide Experimental and Modeling Analysis of Insulin Signaling through Forkhead Box Protein O1 (FOXO1) in Human Adipocytes, Normally and in Type 2 Diabetes.在正常及2型糖尿病状态下,人类脂肪细胞中通过叉头框蛋白O1(FOXO1)进行的胰岛素信号传导的全系统实验与建模分析
J Biol Chem. 2016 Jul 22;291(30):15806-19. doi: 10.1074/jbc.M116.715763. Epub 2016 May 20.
6
Curculigoside and polyphenol-rich ethyl acetate fraction of Molineria latifolia rhizome improved glucose uptake via potential mTOR/AKT activated GLUT4 translocation.密花香薷根茎中毛蕊花糖苷和富含多酚的乙酸乙酯级分通过潜在的 mTOR/AKT 激活的 GLUT4 易位来改善葡萄糖摄取。
J Food Drug Anal. 2018 Oct;26(4):1253-1264. doi: 10.1016/j.jfda.2018.03.003. Epub 2018 Apr 5.
7
Serine 474 phosphorylation is essential for maximal Akt2 kinase activity in adipocytes.丝氨酸 474 磷酸化对于脂肪细胞中 Akt2 激酶活性的最大激活至关重要。
J Biol Chem. 2019 Nov 8;294(45):16729-16739. doi: 10.1074/jbc.RA119.010036. Epub 2019 Sep 22.
8
Chronic inhibition of the mTORC1/S6K1 pathway increases insulin-induced PI3K activity but inhibits Akt2 and glucose transport stimulation in 3T3-L1 adipocytes.mTORC1/S6K1信号通路的长期抑制可增强胰岛素诱导的PI3K活性,但会抑制3T3-L1脂肪细胞中Akt2的活性及葡萄糖转运刺激作用。
Mol Endocrinol. 2010 Apr;24(4):766-78. doi: 10.1210/me.2009-0328. Epub 2010 Mar 4.
9
mTORC1 and mTORC2 regulate insulin secretion through Akt in INS-1 cells.mTORC1 和 mTORC2 通过 Akt 调节 INS-1 细胞的胰岛素分泌。
J Endocrinol. 2013 Jan 2;216(1):21-9. doi: 10.1530/JOE-12-0351. Print 2013 Jan.
10
Reciprocal regulation of mTOR complexes in pancreatic islets from humans with type 2 diabetes.2型糖尿病患者胰岛中mTOR复合物的相互调节
Diabetologia. 2017 Apr;60(4):668-678. doi: 10.1007/s00125-016-4188-9. Epub 2016 Dec 21.

引用本文的文献

1
Does GLUT4 Queue? A Mechanistic Mathematical Model for Insulin Response in Adipocytes.葡萄糖转运蛋白4(GLUT4)会排队吗?脂肪细胞中胰岛素反应的机制数学模型。
Bull Math Biol. 2025 Sep 2;87(10):141. doi: 10.1007/s11538-025-01490-6.
2
Trapa Bispinosa Roxb. Inhibits the Insulin-Dependent AKT/WNK1 Pathway to Induce Autophagy in Mice with Type 2 Diabetes.菱角抑制胰岛素依赖的AKT/WNK1通路以诱导2型糖尿病小鼠自噬。
Diabetes Metab Syndr Obes. 2023 Oct 5;16:3095-3104. doi: 10.2147/DMSO.S430132. eCollection 2023.
3
Kullback-Leibler Divergence of an Open-Queuing Network of a Cell-Signal-Transduction Cascade.

本文引用的文献

1
Stochastic Simulation of Cellular Metabolism.细胞代谢的随机模拟
IEEE Access. 2020;8:79734-79744. doi: 10.1109/access.2020.2986833. Epub 2020 Apr 17.
2
Queueing theory model of Krebs cycle.三羧酸循环的排队论模型
Bioinformatics. 2021 Sep 29;37(18):2912-2919. doi: 10.1093/bioinformatics/btab177.
3
A review on genetic algorithm: past, present, and future.关于遗传算法的综述:过去、现在与未来。
细胞信号转导级联开放排队网络的库尔贝克-莱布勒散度
Entropy (Basel). 2023 Feb 10;25(2):326. doi: 10.3390/e25020326.
Multimed Tools Appl. 2021;80(5):8091-8126. doi: 10.1007/s11042-020-10139-6. Epub 2020 Oct 31.
4
How does mTOR sense glucose starvation? AMPK is the usual suspect.mTOR是如何感知葡萄糖饥饿的?通常认为是AMPK在起作用。
Cell Death Discov. 2020 Apr 22;6:27. doi: 10.1038/s41420-020-0260-9. eCollection 2020.
5
mTOR signaling pathway and mTOR inhibitors in cancer: progress and challenges.癌症中的mTOR信号通路与mTOR抑制剂:进展与挑战
Cell Biosci. 2020 Mar 10;10:31. doi: 10.1186/s13578-020-00396-1. eCollection 2020.
6
mTOR is a Key Protein Involved in the Metabolic Effects of Simple Sugars.mTOR 是一种参与简单糖代谢效应的关键蛋白。
Int J Mol Sci. 2019 Mar 5;20(5):1117. doi: 10.3390/ijms20051117.
7
mTORC Inhibitors as Broad-Spectrum Therapeutics for Age-Related Diseases.mTORC 抑制剂作为治疗与年龄相关疾病的广谱疗法。
Int J Mol Sci. 2018 Aug 8;19(8):2325. doi: 10.3390/ijms19082325.
8
Role of mTOR in Glucose and Lipid Metabolism.mTOR 在糖和脂代谢中的作用。
Int J Mol Sci. 2018 Jul 13;19(7):2043. doi: 10.3390/ijms19072043.
9
mTORC1 Signaling: A Double-Edged Sword in Diabetic β Cells.mTORC1 信号通路:糖尿病 β 细胞中的双刃剑。
Cell Metab. 2018 Feb 6;27(2):314-331. doi: 10.1016/j.cmet.2017.11.004. Epub 2017 Dec 21.
10
The Role of Mammalian Target of Rapamycin (mTOR) in Insulin Signaling.哺乳动物雷帕霉素靶蛋白(mTOR)在胰岛素信号转导中的作用。
Nutrients. 2017 Oct 27;9(11):1176. doi: 10.3390/nu9111176.