• 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

间歇性高糖增强INS-1细胞的凋亡。

Intermittent high glucose enhances apoptosis in INS-1 cells.

作者信息

Shi Xiao-li, Ren Yue-zhong, Wu Jing

机构信息

Department of Endocrinology, Second Affiliated Hospital of Medical College, Zhejiang University, Hangzhou 310009, China.

出版信息

Exp Diabetes Res. 2011;2011:754673. doi: 10.1155/2011/754673. Epub 2011 Jun 21.

DOI:10.1155/2011/754673
PMID:21747833
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3124292/
Abstract

To investigate the effect of intermittent high glucose (IHG) and sustained high glucose (SHG) on inducing β-cell apoptosis and the potential involved mechanisms, INS-1 beta cells were incubated for 72 h in the medium containing different glucose concentrations: control (5.5 mmol/L), SHG (33.3 mmol/L), and IHG (5.5 mmol/L and 33.3 mmol/L glucose alternating every 12 h). Cell viability, apoptosis rate, and oxidative-stress markers were determined. The results showed that the apoptosis induced by IHG was more obvious than that by SHG. Simultaneously, the intracellular level of oxidative stress was more significantly increased in INS-1 cells exposed to IHG. These findings suggest that intermittent high glucose could be more deleterious to β-cell than a constant high concentration of glucose, this may be due to the aggravation of oxidative stress triggered by intermittent high glucose.

摘要

为研究间歇性高糖(IHG)和持续性高糖(SHG)对诱导β细胞凋亡的影响及其潜在机制,将INS-1β细胞在含有不同葡萄糖浓度的培养基中培养72小时:对照组(5.5 mmol/L)、SHG组(33.3 mmol/L)和IHG组(5.5 mmol/L和33.3 mmol/L葡萄糖每12小时交替一次)。测定细胞活力、凋亡率和氧化应激标志物。结果显示,IHG诱导的凋亡比SHG更明显。同时,暴露于IHG的INS-1细胞内氧化应激水平显著升高。这些发现表明,间歇性高糖可能比持续高浓度葡萄糖对β细胞更具危害性,这可能是由于间歇性高糖引发的氧化应激加剧所致。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/764f/3124292/02dd9e04083e/EDR2011-754673.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/764f/3124292/f4918d817a1b/EDR2011-754673.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/764f/3124292/2ad04d585350/EDR2011-754673.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/764f/3124292/aa9aaeda51d3/EDR2011-754673.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/764f/3124292/02dd9e04083e/EDR2011-754673.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/764f/3124292/f4918d817a1b/EDR2011-754673.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/764f/3124292/2ad04d585350/EDR2011-754673.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/764f/3124292/aa9aaeda51d3/EDR2011-754673.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/764f/3124292/02dd9e04083e/EDR2011-754673.004.jpg

相似文献

1
Intermittent high glucose enhances apoptosis in INS-1 cells.间歇性高糖增强INS-1细胞的凋亡。
Exp Diabetes Res. 2011;2011:754673. doi: 10.1155/2011/754673. Epub 2011 Jun 21.
2
[Impairment of pancreatic islet beta cell function induced by intermittent high glucose through oxidative and endoplasmic reticulum stress: experiment with rat pancreatic islet beta cells].间歇性高糖通过氧化应激和内质网应激诱导大鼠胰岛β细胞功能损伤的实验研究
Zhonghua Yi Xue Za Zhi. 2008 Jul 22;88(28):2002-4.
3
The cytotoxic role of intermittent high glucose on apoptosis and cell viability in pancreatic beta cells.间歇性高糖对胰腺β细胞凋亡和细胞活力的细胞毒性作用。
J Diabetes Res. 2014;2014:712781. doi: 10.1155/2014/712781. Epub 2014 Mar 17.
4
Increase of INS-1 cell apoptosis under glucose fluctuation and the involvement of FOXO-SIRT pathway.葡萄糖波动诱导 INS-1 细胞凋亡增加及 FOXO-SIRT 通路的作用。
Diabetes Res Clin Pract. 2012 Oct;98(1):132-9. doi: 10.1016/j.diabres.2012.04.013. Epub 2012 May 11.
5
Systematic investigation into the role of intermittent high glucose in pancreatic beta-cells.对间歇性高血糖在胰腺β细胞中的作用进行系统研究。
Int J Clin Exp Med. 2015 Apr 15;8(4):5462-9. eCollection 2015.
6
Involvement of chronic stresses in rat islet and INS-1 cell glucotoxicity induced by intermittent high glucose.慢性应激参与间歇性高糖诱导的大鼠胰岛和INS-1细胞糖毒性作用。
Mol Cell Endocrinol. 2008 Sep 10;291(1-2):71-8. doi: 10.1016/j.mce.2008.03.004. Epub 2008 Mar 22.
7
Adiponectin reduces glucotoxicity-induced apoptosis of INS-1 rat insulin-secreting cells on a microfluidic chip.脂联素可减少微流控芯片上葡萄糖毒性诱导的INS-1大鼠胰岛素分泌细胞凋亡。
Tohoku J Exp Med. 2009 Jan;217(1):59-65. doi: 10.1620/tjem.217.59.
8
Ginsenoside Rg3 prevents INS-1 cell death from intermittent high glucose stress.人参皂苷Rg3可预防间歇性高糖应激诱导的INS-1细胞死亡。
Islets. 2016 Apr 18;8(3):57-64. doi: 10.1080/19382014.2016.1161874.
9
[Damage mechanism of intermittent exposure to high concentrations of glucose to beta cell lines (HIT-T15 cell)].[高浓度葡萄糖间歇性暴露对β细胞系(HIT-T15细胞)的损伤机制]
Sichuan Da Xue Xue Bao Yi Xue Ban. 2008 Jan;39(1):69-71, 93.
10
Oscillating high glucose enhances oxidative stress and apoptosis in human coronary artery endothelial cells.波动的高葡萄糖增强了人冠状动脉内皮细胞的氧化应激和细胞凋亡。
J Endocrinol Invest. 2014 Jul;37(7):645-51. doi: 10.1007/s40618-014-0086-5. Epub 2014 May 24.

引用本文的文献

1
Exploring the potential of gemcitabine-metal-organic frameworks in combating pancreatic cancer under ketogenic conditions.探索吉西他滨-金属有机框架在生酮条件下对抗胰腺癌的潜力。
BMC Cancer. 2025 Jan 9;25(1):53. doi: 10.1186/s12885-024-13397-x.
2
Comparative Analysis of Orthosteric and Allosteric GLP-1R Agonists' Effects on Insulin Secretion from Healthy, Diabetic, and Recovered INS-1E Pancreatic Beta Cells.正构和变构 GLP-1R 激动剂对健康、糖尿病和恢复的 INS-1E 胰腺β细胞胰岛素分泌作用的比较分析。
Int J Mol Sci. 2024 Jun 7;25(12):6331. doi: 10.3390/ijms25126331.
3
A Comprehensive Review of the Effects of Glycemic Carbohydrates on the Neurocognitive Functions Based on Gut Microenvironment Regulation and Glycemic Fluctuation Control.

本文引用的文献

1
Involvement of osteopontin upregulation on mesangial cells growth and collagen synthesis induced by intermittent high glucose.间歇性高糖诱导的骨桥蛋白上调对系膜细胞增殖和胶原合成的作用。
J Cell Biochem. 2010 Apr 15;109(6):1210-21. doi: 10.1002/jcb.22503.
2
Transient high glucose causes persistent epigenetic changes and altered gene expression during subsequent normoglycemia.短暂性高血糖会导致后续血糖正常期间持续的表观遗传变化和基因表达改变。
J Exp Med. 2008 Sep 29;205(10):2409-17. doi: 10.1084/jem.20081188. Epub 2008 Sep 22.
3
Glucose and leptin induce apoptosis in human beta-cells and impair glucose-stimulated insulin secretion through activation of c-Jun N-terminal kinases.
基于肠道微环境调控和血糖波动控制的血糖碳水化合物对神经认知功能影响的综合评价
Nutrients. 2023 Dec 12;15(24):5080. doi: 10.3390/nu15245080.
4
Chronic and Intermittent Hyperglycemia Modulates Expression of Key Molecules of PI3K/AKT Pathway in Differentiating Human Visceral Adipocytes.慢性和间歇性高血糖调节人内脏脂肪细胞分化过程中 PI3K/AKT 通路关键分子的表达。
Int J Mol Sci. 2021 Jul 19;22(14):7712. doi: 10.3390/ijms22147712.
5
iGlarLixi reduces residual hyperglycemia in Japanese patients with type 2 diabetes uncontrolled on basal insulin: A post-hoc analysis of the LixiLan JP-L trial.利西拉来联合甘精胰岛素降低血糖控制不佳的日本 2 型糖尿病患者的残余血糖:来自 LixiLan JP-L 试验的事后分析。
J Diabetes Investig. 2021 Nov;12(11):1992-2001. doi: 10.1111/jdi.13563. Epub 2021 Jun 19.
6
Molecular Mechanisms of Glucose Fluctuations on Diabetic Complications.血糖波动对糖尿病并发症的分子机制
Front Endocrinol (Lausanne). 2019 Sep 18;10:640. doi: 10.3389/fendo.2019.00640. eCollection 2019.
7
Hypericin maintians PDX1 expression via the Erk pathway and protects islet β-cells against glucotoxicity and lipotoxicity.金丝桃素通过 Erk 通路维持 PDX1 的表达,保护胰岛 β 细胞免受糖毒性和脂毒性的损害。
Int J Biol Sci. 2019 Jun 2;15(7):1472-1487. doi: 10.7150/ijbs.33817. eCollection 2019.
8
Bisoprolol protects myocardium cells against ischemia/reperfusion injury by attenuating unfolded protein response in rats.比索洛尔通过减轻大鼠未折叠蛋白反应来保护心肌细胞免受缺血/再灌注损伤。
Sci Rep. 2017 Sep 19;7(1):11859. doi: 10.1038/s41598-017-12366-8.
9
Docosahexaenoic Acid Inhibits Vascular Smooth Muscle Cell Proliferation Induced by Glucose Variability.二十二碳六烯酸抑制葡萄糖变异性诱导的血管平滑肌细胞增殖。
Open Biochem J. 2017 Jun 30;11:56-65. doi: 10.2174/1874091X01711010056. eCollection 2017.
10
Puerarin may protect against Schwann cell damage induced by glucose fluctuation.葛根素可能对葡萄糖波动诱导的雪旺细胞损伤具有保护作用。
J Nat Med. 2017 Jul;71(3):472-481. doi: 10.1007/s11418-016-1067-0. Epub 2017 Feb 8.
葡萄糖和瘦素可诱导人β细胞凋亡,并通过激活c-Jun氨基末端激酶损害葡萄糖刺激的胰岛素分泌。
FASEB J. 2008 Jun;22(6):1905-13. doi: 10.1096/fj.07-101824. Epub 2008 Feb 8.
4
Long-range correlated glucose fluctuations in diabetes.糖尿病中的长程相关葡萄糖波动
Methods Inf Med. 2007;46(2):222-6.
5
Pancreatic B-cell function is altered by oxidative stress induced by acute hyperglycaemia.急性高血糖诱导的氧化应激会改变胰腺β细胞功能。
Diabet Med. 2007 Feb;24(2):154-60. doi: 10.1111/j.1464-5491.2007.02058.x.
6
Long-term effect of the Internet-based glucose monitoring system on HbA1c reduction and glucose stability: a 30-month follow-up study for diabetes management with a ubiquitous medical care system.基于互联网的血糖监测系统对糖化血红蛋白降低及血糖稳定性的长期影响:一项使用普及医疗系统进行糖尿病管理的30个月随访研究。
Diabetes Care. 2006 Dec;29(12):2625-31. doi: 10.2337/dc05-2371.
7
Gliclazide protects human islet beta-cells from apoptosis induced by intermittent high glucose.格列齐特可保护人胰岛β细胞免受间歇性高糖诱导的细胞凋亡。
Diabetes Metab Res Rev. 2007 Mar;23(3):234-8. doi: 10.1002/dmrr.680.
8
Repetitive fluctuations in blood glucose enhance monocyte adhesion to the endothelium of rat thoracic aorta.血糖的反复波动会增强单核细胞对大鼠胸主动脉内皮的黏附。
Arterioscler Thromb Vasc Biol. 2006 Oct;26(10):2275-80. doi: 10.1161/01.ATV.0000239488.05069.03. Epub 2006 Aug 3.
9
Activation of oxidative stress by acute glucose fluctuations compared with sustained chronic hyperglycemia in patients with type 2 diabetes.与2型糖尿病患者持续性慢性高血糖相比,急性血糖波动对氧化应激的激活作用。
JAMA. 2006 Apr 12;295(14):1681-7. doi: 10.1001/jama.295.14.1681.
10
Temporary hyperglycaemia provokes monocyte adhesion to endothelial cells in rat thoracic aorta.短暂性高血糖会引发大鼠胸主动脉中单核细胞与内皮细胞的黏附。
Diabetologia. 2005 Dec;48(12):2667-74. doi: 10.1007/s00125-005-0005-6. Epub 2005 Nov 8.