Candeias Emanuel Monteiro, Sebastião Inês Carolina, Cardoso Susana Maria, Correia Sónia Catarina, Carvalho Cristina Isabel, Plácido Ana Isabel, Santos Maria Sancha, Oliveira Catarina Resende, Moreira Paula Isabel, Duarte Ana Isabel
Emanuel Monteiro Candeias, Inês Carolina Sebastião, Susana Maria Cardoso, Sónia Correia Correia, Cristina Isabel Carvalho, Ana Isabel Plácido, Maria Sancha Santos, Catarina Resende Oliveira, Paula Isabel Moreira, Ana Isabel Duarte, CNC - Center for Neuroscience and Cell Biology, Rua Larga, Faculty of Medicine (1 Floor), University of Coimbra, 3004-517 Coimbra, Portugal.
World J Diabetes. 2015 Jun 25;6(6):807-27. doi: 10.4239/wjd.v6.i6.807.
Long-acting glucagon-like peptide-1 (GLP-1) analogues marketed for type 2 diabetes (T2D) treatment have been showing positive and protective effects in several different tissues, including pancreas, heart or even brain. This gut secreted hormone plays a potent insulinotropic activity and an important role in maintaining glucose homeostasis. Furthermore, growing evidences suggest the occurrence of several commonalities between T2D and neurodegenerative diseases, insulin resistance being pointed as a main cause for cognitive decline and increased risk to develop dementia. In this regard, it has also been suggested that stimulation of brain insulin signaling may have a protective role against cognitive deficits. As GLP-1 receptors (GLP-1R) are expressed throughout the central nervous system and GLP-1 may cross the blood-brain-barrier, an emerging hypothesis suggests that they may be promising therapeutic targets against brain dysfunctional insulin signaling-related pathologies. Importantly, GLP-1 actions depend not only on the direct effect mediated by its receptor activation, but also on the gut-brain axis involving an exchange of signals between both tissues via the vagal nerve, thereby regulating numerous physiological functions (e.g., energy homeostasis, glucose-dependent insulin secretion, as well as appetite and weight control). Amongst the incretin/GLP-1 mimetics class of anti-T2D drugs with an increasingly described neuroprotective potential, the already marketed liraglutide emerged as a GLP-1R agonist highly resistant to dipeptidyl peptidase-4 degradation (thereby having an increased half-life) and whose systemic GLP-1R activity is comparable to that of native GLP-1. Importantly, several preclinical studies showed anti-apoptotic, anti-inflammatory, anti-oxidant and neuroprotective effects of liraglutide against T2D, stroke and Alzheimer disease (AD), whereas several clinical trials, demonstrated some surprising benefits of liraglutide on weight loss, microglia inhibition, behavior and cognition, and in AD biomarkers. Herein, we discuss the GLP-1 action through the gut-brain axis, the hormone's regulation of some autonomic functions and liraglutide's neuroprotective potential.
用于治疗2型糖尿病(T2D)的长效胰高血糖素样肽-1(GLP-1)类似物已在包括胰腺、心脏甚至大脑在内的多种不同组织中显示出积极和保护作用。这种由肠道分泌的激素具有强大的促胰岛素分泌活性,在维持葡萄糖稳态中发挥重要作用。此外,越来越多的证据表明T2D与神经退行性疾病之间存在一些共性,胰岛素抵抗被认为是认知能力下降和患痴呆症风险增加的主要原因。在这方面,也有人提出刺激大脑胰岛素信号传导可能对认知缺陷具有保护作用。由于GLP-1受体(GLP-1R)在整个中枢神经系统中均有表达,且GLP-1可能穿过血脑屏障,因此一个新出现的假说是,它们可能是针对与大脑胰岛素信号传导功能失调相关疾病的有前景的治疗靶点。重要的是,GLP-1的作用不仅取决于其受体激活介导的直接效应,还取决于肠-脑轴,该轴涉及通过迷走神经在两个组织之间进行信号交换,从而调节多种生理功能(如能量稳态、葡萄糖依赖性胰岛素分泌以及食欲和体重控制)。在具有越来越多神经保护潜力描述的肠促胰岛素/GLP-1模拟物类抗T2D药物中,已上市的利拉鲁肽是一种对二肽基肽酶-4降解具有高度抗性(从而半衰期延长)的GLP-1R激动剂,其全身GLP-1R活性与天然GLP-1相当。重要的是,多项临床前研究表明利拉鲁肽对T2D、中风和阿尔茨海默病(AD)具有抗凋亡、抗炎、抗氧化和神经保护作用,而多项临床试验证明利拉鲁肽在体重减轻、小胶质细胞抑制、行为和认知以及AD生物标志物方面有一些惊人的益处。在此,我们讨论GLP-1通过肠-脑轴的作用、该激素对某些自主功能的调节以及利拉鲁肽的神经保护潜力。