Physical exercise (PE) can mitigate fine particulate matter (PM 2.5 )-associated metabolic disorders, but its impacts on adipose mitochondrial health under PM 2.5 exposure remain unclear. Here, we performed a 4-month exposure study in C57BL/6 mice (filtered air, PM 2.5 , and PM 2.5 plus PE) and evaluated systemic metabolic phenotypes (body and adipose weights, serum lipids, intraperitoneal glucose tolerance test, and intraperitoneal insulin tolerance test), adipose mitochondrial ultrastructure, and mitochondrial proteomes in brown adipose tissue (BAT) and epididymal white adipose tissue (eWAT). PM 2.5 exposure reduced mitochondrial number and area and caused ultrastructural injury in both adipose depots, accompanied by impaired glucose homeostasis. PE attenuated these phenotypic alterations but did not fully normalize them. Mitochondrial proteomics combined with an integrative stepwise analytical framework identified 6 candidate effector proteins in BAT and 18 in eWAT whose abundance patterns were consistent with PM 2.5 injury and partial PE restoration. Functional annotation suggested enrichment in pathways related to gene expression and protein homeostasis, membrane stability, and respiratory chain assembly in BAT, and protein sorting, post-translational modification, antioxidant activity, ion homeostasis, and energy metabolism in eWAT. These findings suggest that PE may alleviate PM 2.5 -associated adipose mitochondrial dysfunction through coordinated changes across multiple pathways in a tissue-specific manner. • Chronic (4-month) PM 2.5 exposure led to adipose mitochondrial dysfunction. • Regular PE can alleviate PM 2.5 -induced adipose mitochondrial damage. • The effects of PE were tissue-specific and coordinated effects of multiple pathways. • The protective effects of PE against PM 2.5 -induced damage were not incomplete. • PE combined with other strategies may eliminate PM 2.5 -induced injuries.
Nan et al. (Fri,) studied this question.