Laboratory of Neurobiology of Inflammatory and Metabolic Processes, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNISUL), Tubarão, Santa Catarina, Brazil.
Laboratory of Neurology, Graduate Program in Health Sciences, University of Extreme South Santa Catarina (UNESC), Criciúma, Santa Catarina, Brazil.
Neurochem Res. 2023 Nov;48(11):3316-3326. doi: 10.1007/s11064-023-04000-z. Epub 2023 Jul 27.
Excessive consumption of nutrients, as well as obesity, leads to an inflammatory process, especially in adipose tissue. This inflammation reaches the systemic level and, subsequently, the central nervous system (CNS), which can lead to oxidative stress and mitochondrial dysfunction, resulting in brain damage. Thus, adequate treatment for obesity is necessary, including lifestyle changes (diet adequation and physical activity) and pharmacotherapy. However, these drugs can adversely affect the individual's health. In this sense, searching for new therapeutic alternatives for reestablishing metabolic homeostasis is necessary. L-carnitine (LC) and acetyl-L-carnitine (LAC) have neuroprotective effects against oxidative stress and mitochondrial dysfunction in several conditions, including obesity. Therefore, this study aimed to conduct a narrative review of the literature on the effect of LC and LAC on brain damage caused by obesity, in particular, on mitochondrial dysfunction and oxidative stress. Overall, these findings highlight that LC and LAC may be a promising treatment for recovering REDOX status and mitochondrial dysfunction in the CNS in obesity. Future work should focus on better elucidating the molecular mechanisms behind this treatment.
营养物质的过度消耗,以及肥胖,会导致炎症过程,特别是在脂肪组织中。这种炎症会达到全身水平,随后到达中枢神经系统(CNS),这可能导致氧化应激和线粒体功能障碍,从而导致大脑损伤。因此,肥胖的充分治疗包括生活方式的改变(饮食和体育锻炼)和药物治疗。然而,这些药物会对个体的健康产生不良影响。在这种情况下,有必要寻找新的治疗选择,以重新建立代谢稳态。左旋肉碱(LC)和乙酰左旋肉碱(LAC)在几种情况下对氧化应激和线粒体功能障碍具有神经保护作用,包括肥胖。因此,本研究旨在对 LC 和 LAC 对肥胖引起的脑损伤,特别是对线粒体功能障碍和氧化应激的影响进行文献综述。总的来说,这些发现强调了 LC 和 LAC 可能是恢复肥胖时 CNS 氧化还原状态和线粒体功能障碍的有希望的治疗方法。未来的工作应集中在更好地阐明这种治疗背后的分子机制。