Diesel exhaust particles alter adipose mitochondria bioenergetics

Abstract

Diesel exhaust particles (DEP) constitute a significant quantity of air pollution that infiltrate the bloodstream to drive systemic pathologies. While some pathologies are obvious, such as COPD and heart failure, others are less apparent, such as insulin resistance, diabetes, and even obesity. In every case, a role for the receptor of advanced glycation end-products (RAGE) has been implicated. RAGE are cell surface receptors that are implicated in pathological processes, such as inflammation and diabetic complications. Despite the known connection between DEP and metabolic disorders, the effects of DEP exposure on adipose tissue mitochondrial function is unknown. To understand the potential role of RAGE signaling in the context of adipose tissue DEP exposure, mice were nasally exposed to either room air, nebulized diesel exhaust particles, or nebulized diesel exhaust particles + semi-synthetic glycosaminoglycan ethers (SAGEs, RAGE signaling inhibitors) every weekday for three weeks. Inguinal adipose tissue samples were obtained following exposure, and mitochondrial respiration rates were measured. In mice exposed to DEP or DEP + SAGE, mitochondrial respiration of inguinal adipose tissue was not significantly different compared to the room air control mice with the addition of glutamate and malate or ADP. However, respiration was significantly increased with the addition of succinate and FCCP in the inguinal adipose tissue from mice exposed to DEP. The results of this work indicate that DEP exposure elicits a negative effect on adipose mitochondrial respiration. This work was supported in part by funding from Levels Health (BTB) and the National Institutes of Health (NIH 1R15-HL152257, PRR and BTB). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.