Tissue & cell · 2026
Oxidative stress and mitochondrial dysfunction contribute to pulmonary impairment in a murine model of type 2 diabetes mellitus.
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Bansal Rohit, Akhil Akhil, Kumari Preety, Naura Amarjit S, Bhatnagar Archana
Аннотация
BACKGROUND: Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by hyperglycemia, insulin resistance, and partial pancreatic β-cell destruction. While diabetic complications affecting the cardiovascular, renal, and nervous systems are well-known, pulmonary dysfunction remains understudied. Emerging evidence links diabetes to impaired pulmonary structure, function via oxidative stress and mitochondrial dysfunction.
METHODOLOGY: A T2DM model was developed using C57BL6/J male mice fed a high-fat diet and treated with streptozotocin. Pulmonary function was assessed using dual-chamber plethysmography. Biochemical, inflammatory, and oxidative stress markers were analyzed in serum and lung tissue. Antioxidant enzyme activities (MnSOD and catalase) and mitochondrial dysfunction were evaluated in lung tissue lysate and mitochondrial extract. Protein markers related to energy metabolism (AMPK, AKT, PGC-1α, and HO-1) were studied in single-cell lung tissue cultures.
RESULTS: T2DM mice exhibited hyperphagia, polydipsia, elevated liver enzymes, dyslipidemia, and increased inflammatory cytokines (IL-17A, IL-1β, IFN-γ). Pulmonary tissues showed heightened oxidative stress, reduced antioxidant enzyme activity, and mitochondrial dysfunction, accompanied by significant alterations in AMPK, AKT, PGC-1α, and HO-1 expression.
CONCLUSION: T2DM significantly impairs lung function by inducing oxidative damage, mitochondrial dysfunction, and metabolic disruptions in lung. These findings underscore the systemic impact of diabetes and highlight need for therapeutic strategies targeting oxidative stress and mitochondrial health to mitigate pulmonary complications in T2DM.
METHODOLOGY: A T2DM model was developed using C57BL6/J male mice fed a high-fat diet and treated with streptozotocin. Pulmonary function was assessed using dual-chamber plethysmography. Biochemical, inflammatory, and oxidative stress markers were analyzed in serum and lung tissue. Antioxidant enzyme activities (MnSOD and catalase) and mitochondrial dysfunction were evaluated in lung tissue lysate and mitochondrial extract. Protein markers related to energy metabolism (AMPK, AKT, PGC-1α, and HO-1) were studied in single-cell lung tissue cultures.
RESULTS: T2DM mice exhibited hyperphagia, polydipsia, elevated liver enzymes, dyslipidemia, and increased inflammatory cytokines (IL-17A, IL-1β, IFN-γ). Pulmonary tissues showed heightened oxidative stress, reduced antioxidant enzyme activity, and mitochondrial dysfunction, accompanied by significant alterations in AMPK, AKT, PGC-1α, and HO-1 expression.
CONCLUSION: T2DM significantly impairs lung function by inducing oxidative damage, mitochondrial dysfunction, and metabolic disruptions in lung. These findings underscore the systemic impact of diabetes and highlight need for therapeutic strategies targeting oxidative stress and mitochondrial health to mitigate pulmonary complications in T2DM.