Poor glycaemic control in type 2 diabetes compromises leukocyte oxygen consumption rate, OXPHOS complex content and neutrophil-endothelial interactions

The mitochondrial electron transport chain becomes overloaded in type 2 diabetes (T2D), which increases ROS (Reactive Oxygen Species) production and impairs mitochondrial function. Peripheral blood mononuclear cells (PBMCs) are critical players in the inflammatory process that underlies T2D. Poor gl...

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Published in:Redox biology 2025-01, p.103516, Article 103516
Main Authors: Cacace, Julia, Luna-Marco, Clara, Hermo-Argibay, Alberto, Pesantes-Somogyi, Catherine, Hernández-López, Omar A., Pelechá-Salvador, María, Bañuls, Celia, Apostolova, Nadezda, de Miguel-Rodríguez, Luis, Morillas, Carlos, Rocha, Milagros, Rovira-Llopis, Susana, Víctor, Víctor M.
Format: Article
Language:English
Subjects:
HbA1c
inflammation
mitochondria
OXPHOS
type 2 diabetes
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Summary:The mitochondrial electron transport chain becomes overloaded in type 2 diabetes (T2D), which increases ROS (Reactive Oxygen Species) production and impairs mitochondrial function. Peripheral blood mononuclear cells (PBMCs) are critical players in the inflammatory process that underlies T2D. Poor glycaemic control in T2D is closely linked to the development of comorbidities. Our aim was to evaluate if glycaemic control in T2D has an impact on the oxygen consumption rates (OCR) of PBMC, OXPHOS complexes and inflammation. We recruited 181 subjects, consisting of 79 healthy controls, 64 patients with T2D and good glycaemic control (HbA1c7%). We found a decrease in the basal OCR of PBMCs from patients with HbA1c>7% with respect to controls (p7% than in controls and patients with HbA1c
ISSN:2213-2317
2213-2317
DOI:10.1016/j.redox.2025.103516