文章基本信息

标题：Reduced mitochondrial respiration in T cells of patients with major depressive disorder
本地全文：下载
作者：Stefanie Gamradt ; Helge Hasselmann ; Aline Taenzer 等
期刊名称：iScience
印刷版ISSN：2589-0042
出版年度：2021
卷号：24
期号：11
页码：1-19
DOI：10.1016/j.isci.2021.103312
语种：English
出版社：Elsevier
摘要：SummaryConverging evidence indicates that major depressive disorder (MDD) and metabolic disorders might be mediated by shared (patho)biological pathways. However, the converging cellular and molecular signatures remain unknown. Here, we investigated metabolic dysfunction on a systemic, cellular, and molecular level in unmedicated patients with MDD compared with matched healthy controls (HC). Despite comparable BMI scores and absence of cardiometabolic disease, patients with MDD presented with significant dyslipidemia. On a cellular level, T cells obtained from patients with MDD exhibited reduced respiratory and glycolytic capacity. Gene expression analysis revealed increased carnitine palmitoyltransferase IA (CPT1a) levels in T cells, the rate-limiting enzyme for mitochondrial long-chain fatty acid oxidation. Together, our results indicate metabolic dysfunction in unmedicated, non-overweight patients with MDD on a systemic, cellular, and molecular level. This evidence for reduced mitochondrial respiration in T cells of patients with MDD provides translation of previous animal studies regarding a putative role of altered immunometabolism in depression pathobiology.Graphical abstractDisplay OmittedHighlights•MDD patients display signs of metabolic imbalance on a systemic level•Mitochondrial respiration and glycolysis are decreased in T cells of MDD patients•Key cellular metabolic markers negatively correlate with depression severity•Increased expression of CPT1a in T cells correlates with many serum metabolitesCellular neuroscience; Immunology; Metabolomics