Department of Neurology, University of Medicine, Pharmacy, Science and Technology of Târgu Mureș 'George Emil Palade', 540142 Târgu Mureș, Romania.
1st Neurology Clinic, Mures County Clinical Emergency Hospital, 540136 Târgu Mureș, Romania.
Int J Mol Sci. 2024 May 7;25(10):5059. doi: 10.3390/ijms25105059.
Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by progressive loss of motor neurons. Emerging evidence suggests a potential link between metabolic dysregulation and ALS pathogenesis. This study aimed to investigate the relationship between metabolic hormones and disease progression in ALS patients. A cross-sectional study was conducted involving 44 ALS patients recruited from a tertiary care center. Serum levels of insulin, total amylin, C-peptide, active ghrelin, GIP (gastric inhibitory peptide), GLP-1 active (glucagon-like peptide-1), glucagon, PYY (peptide YY), PP (pancreatic polypeptide), leptin, interleukin-6, MCP-1 (monocyte chemoattractant protein-1), and TNFα (tumor necrosis factor alpha) were measured, and correlations with ALSFRS-R, evolution scores, and biomarkers were analyzed using Spearman correlation coefficients. Subgroup analyses based on ALS subtypes, progression pattern of disease, and disease progression rate patterns were performed. Significant correlations were observed between metabolic hormones and ALS evolution scores. Insulin and amylin exhibited strong correlations with disease progression and clinical functional outcomes, with insulin showing particularly robust associations. Other hormones such as C-peptide, leptin, and GLP-1 also showed correlations with ALS progression and functional status. Subgroup analyses revealed differences in hormone levels based on sex and disease evolution patterns, with male patients showing higher amylin and glucagon levels. ALS patients with slower disease progression exhibited elevated levels of amylin and insulin. Our findings suggest a potential role for metabolic hormones in modulating ALS progression and functional outcomes. Further research is needed to elucidate the underlying mechanisms and explore the therapeutic implications of targeting metabolic pathways in ALS management.
肌萎缩侧索硬化症（ALS）是一种破坏性的神经退行性疾病，其特征是运动神经元进行性丧失。新出现的证据表明代谢失调与 ALS 发病机制之间存在潜在联系。本研究旨在探讨代谢激素与 ALS 患者疾病进展之间的关系。进行了一项横断面研究，共纳入了 44 名来自三级保健中心的 ALS 患者。测量了血清胰岛素、总淀粉样蛋白、C 肽、活性胃饥饿素、GIP（胃抑制肽）、GLP-1 活性（胰高血糖素样肽-1）、胰高血糖素、PYY（肽 YY）、PP（胰腺多肽）、瘦素、白细胞介素-6、MCP-1（单核细胞趋化蛋白-1）和 TNFα（肿瘤坏死因子-α）的水平，并使用 Spearman 相关系数分析了它们与 ALSFRS-R、进化评分和生物标志物的相关性。根据 ALS 亚型、疾病进展模式和疾病进展率模式进行了亚组分析。代谢激素与 ALS 进化评分之间存在显著相关性。胰岛素和淀粉样蛋白与疾病进展和临床功能结局具有很强的相关性，其中胰岛素相关性尤其显著。其他激素，如 C 肽、瘦素和 GLP-1，也与 ALS 进展和功能状态相关。亚组分析显示，激素水平存在基于性别和疾病进化模式的差异，男性患者的淀粉样蛋白和胰高血糖素水平较高。疾病进展较慢的 ALS 患者表现出较高的淀粉样蛋白和胰岛素水平。我们的研究结果表明，代谢激素在调节 ALS 进展和功能结局方面可能发挥作用。需要进一步研究阐明潜在机制，并探讨靶向代谢途径在 ALS 管理中的治疗意义。
