GLP1-R agonists

  • 文章类型: Letter
    暂无摘要。
    导出

    更多引用

    收藏

    翻译标题摘要

    我要上传

    求助全文

  • 文章类型: Journal Article
    缺氧缺血性脑病(HIE)是由于分娩过程中新生儿大脑的血流量和氧气减少引起的。导致婴儿死亡或严重的脑损伤,全球发病率为每1000例活产1.5例。胰高血糖素样肽1受体(GLP1-R)激动剂,用于2型糖尿病的治疗,在各种脑损伤模型中表现出神经保护作用,包括HIE.在这项研究中,我们观察到,在出生后第10天,手术诱导的缺氧缺血性(HI)脑损伤小鼠,在立即全身给药exendin-4或斯马鲁肽后,神经系统结局增强.短期和长期评估显示神经病理学改善,存活率,和运动功能。我们探索了GLP1-R激动剂触发神经保护和减少新生小鼠氧糖剥夺和HI后炎症的机制。强调PI3/AKT信号通路的上调和cAMP水平的升高。这些发现揭示了GLP1-R激动剂在HIE中的神经保护和抗炎作用。可能延伸到其他神经系统疾病,支持他们在治疗HIE婴儿方面的潜在临床应用。
    Hypoxic-ischaemic encephalopathy (HIE) arises from diminished blood flow and oxygen to the neonatal brain during labor, leading to infant mortality or severe brain damage, with a global incidence of 1.5 per 1000 live births. Glucagon-like Peptide 1 Receptor (GLP1-R) agonists, used in type 2 diabetes treatment, exhibit neuroprotective effects in various brain injury models, including HIE. In this study, we observed enhanced neurological outcomes in post-natal day 10 mice with surgically induced hypoxic-ischaemic (HI) brain injury after immediate systemic administration of exendin-4 or semaglutide. Short- and long-term assessments revealed improved neuropathology, survival rates, and locomotor function. We explored the mechanisms by which GLP1-R agonists trigger neuroprotection and reduce inflammation following oxygen-glucose deprivation and HI in neonatal mice, highlighting the upregulation of the PI3/AKT signalling pathway and increased cAMP levels. These findings shed light on the neuroprotective and anti-inflammatory effects of GLP1-R agonists in HIE, potentially extending to other neurological conditions, supporting their potential clinical use in treating infants with HIE.
    导出

    更多引用

    收藏

    翻译标题摘要

    我要上传

       PDF(Pubmed)

  • 文章类型: Journal Article
    帕金森病(PD)是最常见的神经退行性疾病之一。最近的数据强调了神经退行性疾病之间的相似性,包括PD和2型糖尿病(T2DM),表明肠脑轴之间的关键相互作用。胰高血糖素样肽-1受体(GLP-1R)激动剂,以其在T2DM治疗中的应用而闻名,目前作为新型PD改性剂被广泛研究。对于这篇叙述性评论文章,我们在PubMed和Scopus数据库中搜索了同行评审的研究,回顾以英语发表的有关GLP-1R激动剂和PD的文章和临床试验,没有时间限制.我们还筛选了选定文章的参考文献中可能的其他文章,以包括大多数关键的最新证据。许多关于动物模型和临床前研究的数据表明,GLP1-R激动剂可以恢复多巴胺水平,抑制多巴胺能的损失,减轻神经元变性并减轻PD的运动和非运动特征。来自临床研究的证据也非常有希望,增加在目前可用于PD治疗的药物中添加GLP1-R激动剂的可能性。
    Parkinson\'s disease (PD) is one of the most common neurodegenerative diseases. Recent data highlight similarities between neurodegenerative diseases, including PD and type 2 diabetes mellitus (T2DM), suggesting a crucial interplay between the gut-brain axis. Glucagon-like peptide-1 receptor (GLP-1R) agonists, known for their use in T2DM treatment, are currently extensively studied as novel PD modifying agents. For this narrative review article, we searched PubMed and Scopus databases for peer-reviewed research, review articles and clinical trials regarding GLP-1R agonists and PD published in the English language with no time restrictions. We also screened the references of the selected articles for possible additional articles in order to include most of the key recent evidence. Many data on animal models and preclinical studies show that GLP1-R agonists can restore dopamine levels, inhibit dopaminergic loss, attenuate neuronal degeneration and alleviate motor and non-motor features of PD. Evidence from clinical studies is also very promising, enhancing the possibility of adding GLP1-R agonists to the current armamentarium of drugs available for PD treatment.
    导出

    更多引用

    收藏

    翻译标题摘要

    我要上传

       PDF(Pubmed)

  • 文章类型: Journal Article
    Chronic obstructive pulmonary disease (COPD) and type 2 diabetes mellitus (T2DM) often coexist. The mechanistic links between these two diseases are complex, multifactorial, and not entirely understood, but they can influence the approach to treatment. Understanding whether COPD comes first followed by T2DM or vice versa, or whether the two diseases develop simultaneously due to common underlying mechanisms, is important for the development of novel therapeutic approaches to these two important diseases. In this review, we discuss the potential links between COPD and T2DM and pharmacological approaches that might target these links.
    导出

    更多引用

    收藏

    翻译标题摘要

    我要上传

    求助全文

公众号