Fine particulate matter (PM2.5) constitutes a significant component of ambient air pollution that has been implicated in the pathogenesis of metabolic disorders, including insulin resistance and type 2 diabetes. Among PM2.5 constituents, diesel exhaust particles (DEP) are prevalent particulates that infiltrate the bloodstream to drive systemic pathologies. The purpose of this study was to characterize the metabolic response of adipose tissue to DEP. We aimed to provide a comprehensive understanding by exploring mitochondrial bioenergetics, characterizing the inflammatory marker profile, including adipokines, and conducting a detailed histological analysis of adipocytes to provide valuable insights to the evolving understanding of the intricate interplay between pollution and adipose tissue function. Following daily inhalation exposure to DEP in mice, we observed a selective increase in adipose tissue mass and altered mitochondrial respiration in the adipose tissue. Furthermore, we observed increased pro-inflammatory cytokines, changes in adipokine secretion, and alterations in adipose histology reflective of adipocyte hypertrophy. In conclusion, exposure to DEP disrupts adipose tissue function by altering adipocyte mitochondrial function and contributing to inflammation. These novel findings provide valuable insights that may facilitate the development of therapeutic interventions addressing metabolic disorders in the future.
| Identifer | oai:union.ndltd.org:BGMYU2/oai:scholarsarchive.byu.edu:etd-11272 |
| Date | 12 March 2024 |
| Creators | Warren, Cali Elizabeth |
| Publisher | BYU ScholarsArchive |
| Source Sets | Brigham Young University |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | Theses and Dissertations |
| Rights | https://lib.byu.edu/about/copyright/ |
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