Abstract
BackgroundEpidemiological evidence indicates that diabetic patients have increased susceptibility to adverse cardiovascular outcomes related to acute increases in exposures to particulate air pollution. However, mechanisms underlying these effects remain unclear.MethodsTo evaluate the possible mechanisms underlying these actions, we assessed the systemic effects of diesel exhaust particles (DEP) in control mice, and mice with streptozotocin–induced type 1 diabetes. Four weeks following induction of diabetes, the animals were intratracheally instilled (i.t.) with DEP (0.4 mg/kg) or saline, and several cardiovascular endpoints were measured 24 h thereafter.ResultsDEP caused leukocytosis and a significant increase in plasma C-reactive protein and 8-isoprostane concentrations in diabetic mice compared to diabetic mice exposed to saline or non-diabetic mice exposed to DEP. The arterial PO2 as well as the number of platelets and the thrombotic occlusion time in pial arterioles assessed in vivo were significantly decreased following the i.t. instillation of DEP in diabetic mice compared to diabetic mice exposed to saline or non-diabetic mice exposed to DEP. Both alanine aminotransferase and aspartate transaminase activities, as well as the plasma concentrations of plasminogen activator inhibitor and von Willebrand factor were significantly increased in DEP-exposed diabetic mice compared to diabetic mice exposed to saline or DEP-exposed non-diabetic mice. The in vitro addition of DEP (0.25-1 μg/ml) to untreated mouse blood significantly and dose-dependently induced in vitro platelet aggregation, and these effects were exacerbated in blood of diabetic mice.ConclusionThis study has shown that systemic and coagulation events are aggravated by type 1 diabetes in mice, acutely exposed to DEP and has described the possible mechanisms for these actions that may also be relevant to the exacerbation of cardiovascular morbidity accompanying particulate air pollution in diabetic patients.
Highlights
Epidemiological evidence indicates that diabetic patients have increased susceptibility to adverse cardiovascular outcomes related to acute increases in exposures to particulate air pollution
The leukocyte numbers were increased in diabetic mice exposed to diesel exhaust particles (DEP) compared to diabetic mice exposed to saline or non-diabetic mice exposed to DEP
The plasma concentration of c-reactive protein (CRP) was significantly increased following DEP exposure in diabetic mice compared to diabetic mice exposed to saline or non-diabetic mice exposed to DEP (Figure 1B)
Summary
Epidemiological evidence indicates that diabetic patients have increased susceptibility to adverse cardiovascular outcomes related to acute increases in exposures to particulate air pollution. Type 1 diabetes (known as insulin-dependent diabetes or juvenile-onset diabetes) which is caused by a complete deficiency of insulin secretion resulting from a cellular-mediated autoimmune destruction of the β cells of the pancreas. This form represents about 10% of all forms of diagnosed diabetes. It is well known that cardiovascular complications including thrombosis constitute the major cause of morbidity and mortality in both type 1 and type 2 diabetes [7]
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