• 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

相似文献

1
[Synergistic effects of GABA and hypoglycemic drugs].[γ-氨基丁酸与降糖药物的协同作用]
Probl Endokrinol (Mosk). 2023 Aug 30;69(4):61-69. doi: 10.14341/probl13257.
2
Association Between Use of Sodium-Glucose Cotransporter 2 Inhibitors, Glucagon-like Peptide 1 Agonists, and Dipeptidyl Peptidase 4 Inhibitors With All-Cause Mortality in Patients With Type 2 Diabetes: A Systematic Review and Meta-analysis.钠-葡萄糖共转运蛋白 2 抑制剂、胰高血糖素样肽 1 受体激动剂和二肽基肽酶 4 抑制剂与 2 型糖尿病患者全因死亡率的关联:系统评价和荟萃分析。
JAMA. 2018 Apr 17;319(15):1580-1591. doi: 10.1001/jama.2018.3024.
3
Association between use of sodium-glucose cotransporter 2 inhibitors, glucagon-like peptide 1 agonists, and dipeptidyl peptidase 4 inhibitors with kidney outcomes in patients with type 2 diabetes: A systematic review and network meta-analysis.钠-葡萄糖共转运蛋白 2 抑制剂、胰高血糖素样肽 1 激动剂和二肽基肽酶 4 抑制剂与 2 型糖尿病患者肾脏结局的关系:系统评价和网络荟萃分析。
PLoS One. 2022 Apr 14;17(4):e0267025. doi: 10.1371/journal.pone.0267025. eCollection 2022.
4
Myocardial infarction in type 2 diabetes using sodium-glucose co-transporter-2 inhibitors, dipeptidyl peptidase-4 inhibitors or glucagon-like peptide-1 receptor agonists: proportional hazards analysis by deep neural network based machine learning.基于深度学习神经网络的机器学习对 2 型糖尿病使用钠-葡萄糖共转运蛋白 2 抑制剂、二肽基肽酶-4 抑制剂或胰高血糖素样肽-1 受体激动剂的心肌梗死的比例风险分析。
Curr Med Res Opin. 2020 Mar;36(3):403-409. doi: 10.1080/03007995.2019.1706043. Epub 2020 Jan 6.
5
Differential chemistry (structure), mechanism of action, and pharmacology of GLP-1 receptor agonists and DPP-4 inhibitors.胰高血糖素样肽-1受体激动剂和二肽基肽酶-4抑制剂的化学差异(结构)、作用机制及药理学
J Am Pharm Assoc (2003). 2009 Sep-Oct;49 Suppl 1:S16-29. doi: 10.1331/JAPhA.2009.09078.
6
Cost Effectiveness of Sodium-Glucose Cotransporter-2 (SGLT2) Inhibitors, Glucagon-Like Peptide-1 (GLP-1) Receptor Agonists, and Dipeptidyl Peptidase-4 (DPP-4) Inhibitors: A Systematic Review.钠-葡萄糖共转运蛋白 2(SGLT2)抑制剂、胰高血糖素样肽-1(GLP-1)受体激动剂和二肽基肽酶-4(DPP-4)抑制剂的成本效益:系统评价。
Pharmacoeconomics. 2019 Jun;37(6):777-818. doi: 10.1007/s40273-019-00774-9.
7
Newly approved and promising antidiabetic agents.新批准的且有前景的抗糖尿病药物。
Therapie. 2007 Jul-Aug;62(4):293-310. doi: 10.2515/therapie:2007054. Epub 2007 Nov 6.
8
Add-on therapy in metformin-treated patients with type 2 diabetes at moderate cardiovascular risk: a nationwide study.二甲双胍治疗的 2 型糖尿病中伴有中度心血管风险患者的附加治疗:一项全国性研究。
Cardiovasc Diabetol. 2020 Jul 6;19(1):107. doi: 10.1186/s12933-020-01078-5.
9
Inhibition of DPP-4: a new therapeutic approach for the treatment of type 2 diabetes.二肽基肽酶-4的抑制作用:一种治疗2型糖尿病的新方法。
Curr Med Res Opin. 2007 Apr;23(4):919-31. doi: 10.1185/030079906x162746.
10
Incretin-based drugs for type 2 diabetes: Focus on East Asian perspectives.基于肠降血糖素的药物治疗 2 型糖尿病:关注东亚视角。
J Diabetes Investig. 2016 Apr;7 Suppl 1(Suppl 1):102-9. doi: 10.1111/jdi.12490. Epub 2016 Apr 18.

本文引用的文献

1
Triple drug therapy with GABA, sitagliptin, and omeprazole prevents type 1 diabetes onset and promotes its reversal in non-obese diabetic mice.GABA、西他列汀和奥美拉唑三联药物疗法可预防 1 型糖尿病的发生,并促进非肥胖型糖尿病小鼠的逆转。
Front Endocrinol (Lausanne). 2022 Oct 21;13:1028114. doi: 10.3389/fendo.2022.1028114. eCollection 2022.
2
The role of GABA in islet function.GABA 在胰岛功能中的作用。
Front Endocrinol (Lausanne). 2022 Sep 29;13:972115. doi: 10.3389/fendo.2022.972115. eCollection 2022.
3
Correlation between albuminuria and interstitial injury marker reductions associated with SGLT2 inhibitor treatment in diabetic patients with renal dysfunction.在肾功能障碍的糖尿病患者中,SGLT2 抑制剂治疗与白蛋白尿和间质损伤标志物降低的相关性。
Eur J Med Res. 2022 Aug 6;27(1):140. doi: 10.1186/s40001-022-00737-5.
4
Pathobiology of the Klotho Antiaging Protein and Therapeutic Considerations.Klotho抗衰老蛋白的病理生物学及治疗考量
Front Aging. 2022 Jul 12;3:931331. doi: 10.3389/fragi.2022.931331. eCollection 2022.
5
Empagliflozin attenuates neurodegeneration through antioxidant, anti-inflammatory, and modulation of α-synuclein and Parkin levels in rotenone-induced Parkinson's disease in rats.恩格列净通过抗氧化、抗炎以及调节大鼠鱼藤酮诱导的帕金森病中α-突触核蛋白和帕金蛋白水平来减轻神经退行性变。
Saudi Pharm J. 2022 Jun;30(6):863-873. doi: 10.1016/j.jsps.2022.03.005. Epub 2022 Mar 16.
6
The Ameliorative Effect of Empagliflozin in Vigabatrin-Induced Cerebellar/Neurobehavioral Deficits: Targeting mTOR/AMPK/SIRT-1 Signaling Pathways.恩格列净对 vigabatrin 诱导的小脑/神经行为缺陷的改善作用:靶向 mTOR/AMPK/SIRT-1 信号通路。
Molecules. 2022 Jun 7;27(12):3659. doi: 10.3390/molecules27123659.
7
Empagliflozin alleviates endoplasmic reticulum stress and augments autophagy in rotenone-induced Parkinson's disease in rats: Targeting the GRP78/PERK/eIF2α/CHOP pathway and miR-211-5p.恩格列净可减轻鱼藤酮诱导的大鼠帕金森病中的内质网应激并增强自噬:靶向 GRP78/PERK/eIF2α/CHOP 通路和 miR-211-5p。
Chem Biol Interact. 2022 Aug 1;362:110002. doi: 10.1016/j.cbi.2022.110002. Epub 2022 May 30.
8
Liraglutide Is Protective against Brain Injury in Mice with Febrile Seizures by Inhibiting Inflammatory Factors.利拉鲁肽通过抑制炎症因子对发热性惊厥小鼠的脑损伤起保护作用。
Comput Math Methods Med. 2022 Apr 29;2022:7563281. doi: 10.1155/2022/7563281. eCollection 2022.
9
GABA and Fermented L. Extract Enriched with GABA Ameliorate Obesity through Nox4-IRE1α Sulfonation-RIDD-SIRT1 Decay Axis in High-Fat Diet-Induced Obese Mice.GABA 和富含 GABA 的发酵 L. 提取物通过 Nox4-IRE1α 磺化-RIDD-SIRT1 衰减轴改善高脂肪饮食诱导肥胖小鼠的肥胖。
Nutrients. 2022 Apr 18;14(8):1680. doi: 10.3390/nu14081680.
10
SGLT2 Inhibitors: Physiology and Pharmacology.SGLT2 抑制剂:生理学与药理学。
Kidney360. 2021 Sep 17;2(12):2027-2037. doi: 10.34067/KID.0002772021. eCollection 2021 Dec 30.

[γ-氨基丁酸与降糖药物的协同作用]

[Synergistic effects of GABA and hypoglycemic drugs].

作者信息

Tyurenkov I N, Faibisovich T I, Bakulin D A

机构信息

Volgograd State Medical University.

S. M. Kirov Military Medical Academy.

出版信息

Probl Endokrinol (Mosk). 2023 Aug 30;69(4):61-69. doi: 10.14341/probl13257.

DOI:10.14341/probl13257
PMID:37694868
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10520901/
Abstract

Diabetes mellitus (DM) is the leading cause of premature death and disability. Despite a significant number of drugs, the effectiveness of therapy aimed at normalizing the level of glycemia and preventing complications does not fully satisfy doctors and patients. Therefore, the search for new approaches for the prevention and treatment of DM and its complications continues. Significant resources are used to develop new drugs, but recently the possibility of using «old» widely available drugs with newly discovered pleiotropic properties has been substantiated. These may include preparations of gammaaminobutyric acid (GABA) and agents that directly or indirectly activate GABAergic transmission, which have a pronounced pancreatic protective effect, which has been widely discussed in foreign literature over the past 10-15 years. However, there are few such publications in the domestic literature.It has been established that the content of GABA in β-cells in patients with type 1 and type 2 diabetes is reduced and this correlates with the severity of the disease. Genetic suppression of GABA receptors causes a significant decrease in the mass of β-cells and glucose-stimulated insulin secretion, which confirms the importance of GABA in ensuring glucose homeostasis and the advisability of replenishing the GABA deficiency in DM with its additional administration. It has been established that in animals with DM, GABA suppresses apoptosis and stimulates the regeneration of β-cells, increases β-cell mass and insulin production.Experimental data have been obtained indicating a synergistic effect of GABA when combined with glucagon-like peptide-1 (GLP-1) receptor agonists, DPP-4 inhibitors and sodium-glucose cotransporter 2 (SGLT-2) inhibitors, when a more pronounced pancreoprotective effect is observed, due to decrease in oxidative and nitrosative stress, inflammation, increase in the level of Klotho protein, Nrf-2 activity and antioxidant defense enzymes, suppression of NF-kB activity and expression of pro-inflammatory cytokines. As a result, all this leads to a decrease in apoptosis and death of β-cells, an increase in β-cell mass, insulin production and, at the same time, a decrease in glucagon levels and insulin resistance.The review substantiates the feasibility of using GABA and drugs with a positive GABAeric effect in combination with new generation antidiabetic agents: GLP-1 receptor agonists, DPP-4 inhibitors and SGLT-2 inhibitors in order to increase their antidiabetic potential.The search was carried out in the databases Pubmed, eLibrary, Medline. Keywords: diabetes mellitus, gamma-aminobutyric acid, glucagon-like peptide-1, GLP-1 receptor agonists, glucose-dependent insulinotropic peptide, dipeptidyl peptidase inhibitors, sodium-glucose cotransporter 2 inhibitors. The search was carried out from 2000 to 2022, but the review presents the results studies published mainly in the last 3 years, due to the requirements of the journal for the maximum amount of work and the number of sources.

摘要

糖尿病(DM)是过早死亡和残疾的主要原因。尽管有大量药物,但旨在使血糖水平正常化并预防并发症的治疗效果并不能完全令医生和患者满意。因此,寻找预防和治疗DM及其并发症的新方法的工作仍在继续。大量资源被用于开发新药,但最近已证实使用具有新发现的多效性特性的“老”的常用药物的可能性。这些药物可能包括γ-氨基丁酸(GABA)制剂以及直接或间接激活GABA能传递的药物,它们具有显著的胰腺保护作用,在过去10至15年的国外文献中对此进行了广泛讨论。然而,国内文献中此类出版物较少。已确定1型和2型糖尿病患者β细胞中GABA的含量降低,且这与疾病的严重程度相关。对GABA受体的基因抑制会导致β细胞数量和葡萄糖刺激的胰岛素分泌显著减少,这证实了GABA在确保葡萄糖稳态中的重要性以及通过额外给药补充DM中GABA缺乏的合理性。已确定在患有DM的动物中,GABA可抑制细胞凋亡并刺激β细胞再生,增加β细胞数量和胰岛素产生。已获得实验数据表明,GABA与胰高血糖素样肽-1(GLP-1)受体激动剂、二肽基肽酶-4(DPP-4)抑制剂和钠-葡萄糖协同转运蛋白2(SGLT-2)抑制剂联合使用时具有协同作用,此时由于氧化应激和亚硝化应激、炎症的减少,Klotho蛋白水平、Nrf-2活性和抗氧化防御酶的增加,NF-κB活性和促炎细胞因子表达的抑制,观察到更显著的胰腺保护作用。结果,所有这些导致β细胞凋亡和死亡减少,β细胞数量、胰岛素产生增加,同时胰高血糖素水平和胰岛素抵抗降低。该综述证实了将GABA和具有正向GABA能作用的药物与新一代抗糖尿病药物:GLP-1受体激动剂、DPP-4抑制剂和SGLT-2抑制剂联合使用以增加其抗糖尿病潜力的可行性。检索在数据库Pubmed、eLibrary、Medline中进行。关键词:糖尿病、γ-氨基丁酸、胰高血糖素样肽-1、GLP-1受体激动剂、葡萄糖依赖性促胰岛素多肽、二肽基肽酶抑制剂、钠-葡萄糖协同转运蛋白2抑制剂。检索时间为2000年至2022年,但由于期刊对工作量和来源数量的要求,本综述呈现的主要是过去3年发表的研究结果。