Reduced mitochondrial respiration in T cells of patients with major depressive disorder
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Reduced mitochondrial respiration in T cells of patients with major depressive disorder. / Gamradt, Stefanie; Hasselmann, Helge; Taenzer, Aline; Brasanac, Jelena; Stiglbauer, Victoria; Sattler, Arne; Sajitz-Hermstein, Max; Kierszniowska, Sylwia; Ramien, Caren; Nowacki, Jan; Mascarell-Maricic, Lea; Wingenfeld, Katja; Piber, Dominique; Ströhle, Andreas; Kotsch, Katja; Paul, Friedemann; Otte, Christian; Gold, Stefan M.
in: ISCIENCE, Jahrgang 24, Nr. 11, 103312, 19.11.2021.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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T1 - Reduced mitochondrial respiration in T cells of patients with major depressive disorder
AU - Gamradt, Stefanie
AU - Hasselmann, Helge
AU - Taenzer, Aline
AU - Brasanac, Jelena
AU - Stiglbauer, Victoria
AU - Sattler, Arne
AU - Sajitz-Hermstein, Max
AU - Kierszniowska, Sylwia
AU - Ramien, Caren
AU - Nowacki, Jan
AU - Mascarell-Maricic, Lea
AU - Wingenfeld, Katja
AU - Piber, Dominique
AU - Ströhle, Andreas
AU - Kotsch, Katja
AU - Paul, Friedemann
AU - Otte, Christian
AU - Gold, Stefan M
N1 - © 2021 The Authors.
PY - 2021/11/19
Y1 - 2021/11/19
N2 - Converging 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.
AB - Converging 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.
U2 - 10.1016/j.isci.2021.103312
DO - 10.1016/j.isci.2021.103312
M3 - SCORING: Journal article
C2 - 34765928
VL - 24
JO - ISCIENCE
JF - ISCIENCE
SN - 2589-0042
IS - 11
M1 - 103312
ER -