Extensive epidemiological and experimental evidence indicates that obesity is a strong and robust risk factor for the development of type 2 diabetes (T2D) and cardiovascular disease (CVD). Numerous studies have also reported strong associations between ambient air particulate matter (PM) and an increased CVD and T2D risk. However, the mechanism(s) by which obesity and exposure to environmental air pollutants increase the risk of T2D and CVD remain unknown. A common feature underlying these pathological states is a damaged endothelium. Endothelial health is maintained with the participation of endothelial progenitor cells (EPCs). The presence of CVD risk factors has been shown to decrease not only the circulating levels of EPCs, but their ability to stimulate tissue repair, as well. The number of circulating EPCs is decreased in patients with T2D. Furthermore, our previous work demonstrates that exposures to environmental air pollutions decrease the number of circulating EPCs and impair vascular VEGF signaling. Therefore, our ongoing research examines the effects of exposures to fine particulate matter (PM2.5) and volatile (e.g. acrolein) air pollutions as well as obesity on EPC levels and function, endothelial health and vascular resistance to insulin and VEGF to investigate changes leading to the progression of the vascular complications and the metabolic syndrome. Results of these studies will not only advance our understanding of the mechanisms by which environmental air pollutions and obesity affect vascular health, but could also lead to the development of new diagnostic and therapeutic strategies for the treatment and management of CVDs and T2D.
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