Etchegoyen Melisa, Nobile Mariana H, Baez Francisco, Posesorski Barbara, González Julian, Lago Néstor, Milei José, Otero-Losada Matilde
Institute of Cardiological Research, School of Medicine, University of Buenos Aires, Buenos Aires, Argentina.
Institute of Cardiovascular Pathophysiology, School of Medicine, University of Buenos Aires, UBA-CONICET, Buenos Aires, Argentina.
Front Neurosci. 2018 Apr 20;12:196. doi: 10.3389/fnins.2018.00196. eCollection 2018.
Over the years the prevalence of metabolic syndrome (MetS) has drastically increased in developing countries as a major byproduct of industrialization. Many factors, such as the consumption of high-calorie diets and a sedentary lifestyle, bolster the spread of this disorder. Undoubtedly, the massive and still increasing incidence of MetS places this epidemic as an important public health issue. Hereon we revisit another outlook of MetS beyond its classical association with cardiovascular disease (CVD) and Diabetes Mellitus Type 2 (DM2), for MetS also poses a risk factor for the nervous tissue and threatens neuronal function. First, we revise a few essential concepts of MetS pathophysiology. Second, we explore some neuroprotective approaches in MetS pertaining brain hypoxia. The articles chosen for this review range from the years 1989 until 2017; the selection criteria was based on those providing data and exploratory information on MetS as well as those that studied innovative therapeutic approaches. The characteristically impaired metabolic pathways of MetS lead to hyperglycemia, insulin resistance (IR), inflammation, and hypoxia, all closely associated with an overall pro-oxidative status. Oxidative stress is well-known to cause the wreckage of cellular structures and tissue architecture. Alteration of the redox homeostasis and oxidative stress alter the macromolecular array of DNA, lipids, and proteins, in turn disrupting the biochemical pathways necessary for normal cell function. Different neuroprotective strategies are discussed involving lifestyle changes, medication aimed to mitigate MetS cardinal symptoms, and treatments targeted toward reducing oxidative stress. It is well-known that the routine practice of physical exercise, aerobic activity in particular, and a complete and well-balanced nutrition are key factors to prevent MetS. Nevertheless, pharmacological control of MetS as a whole and pertaining hypertension, dyslipidemia, and endothelial injury contribute to neuronal health improvement. The development of MetS has risen as a risk factor for neurological disorders. The therapeutic strategies include multidisciplinary approaches directed to address different pathological pathways all in concert.
多年来,作为工业化的一个主要副产品,代谢综合征(MetS)在发展中国家的患病率急剧上升。许多因素,如高热量饮食的摄入和久坐不动的生活方式,助长了这种疾病的传播。毫无疑问,MetS的大量且仍在增加的发病率使其成为一个重要的公共卫生问题。在此,我们重新审视MetS的另一个观点,即除了其与心血管疾病(CVD)和2型糖尿病(DM2)的经典关联之外,MetS也是神经组织的一个危险因素,并威胁神经元功能。首先,我们回顾一下MetS病理生理学的一些基本概念。其次,我们探讨一些与脑缺氧相关的MetS中的神经保护方法。本综述所选文章的时间跨度从1989年到2017年;选择标准基于那些提供有关MetS的数据和探索性信息以及那些研究创新治疗方法的文章。MetS典型的受损代谢途径会导致高血糖、胰岛素抵抗(IR)、炎症和缺氧,所有这些都与整体的促氧化状态密切相关。众所周知,氧化应激会导致细胞结构和组织结构的破坏。氧化还原稳态的改变和氧化应激会改变DNA、脂质和蛋白质的大分子排列,进而扰乱正常细胞功能所需的生化途径。本文讨论了不同的神经保护策略,包括生活方式的改变、旨在减轻MetS主要症状的药物治疗以及针对降低氧化应激的治疗。众所周知,体育锻炼,特别是有氧运动的日常实践以及完整且均衡的营养是预防MetS的关键因素。然而,对MetS整体以及与之相关的高血压、血脂异常和内皮损伤的药物控制有助于改善神经元健康。MetS的发展已成为神经疾病的一个危险因素。治疗策略包括针对不同病理途径协同发挥作用的多学科方法。