Recent experimental data have provided associations between ambient PM2.5 (fine particulate matter; diameter ≤ 2.5 μm) and propensity to inflammation and chronic diseases especially among susceptible groups, such as elderly people. There is cumulative evidence that type-2 diabetes mellitus is a chronic inflammatory state aggravated by factors that promote endothelium inflammation. Accordingly our hypothesis that the exposure of aged obese population to PM2.5 might aggravate type-2 diabetes, we used a model of aged, diet-induced obese mice. C57BL6 male mice were fed with regular chow (n=30; RC) or high-fat chow (n=36; HF) during one-year and randomly assigned to filtered (FA-RC, n=16; FA-HF, n=19) or PM2.5 concentrated air (600 μg.m-3) (EXP-RC, n=14; EXPHF, n=17) chambers to have a daily 1 hour exposition during consecutive 30- days. Fast glycemia was measured before the animals were euthanized. The Institution’s Ethics Committee approved all experimental procedures. Heart mRNA content of selected migration, signalization and adhesion proteins were measured by SYBR Green fluorescence Real Time RT-PCR protocol using appropriate primers. There were no difference between RC-EXP and RC-FA nor between HF-EXP and HF-FA body weight. Regarding fast glycemia, both, RC and HF groups, were diabetic, but only the HF group was affected by acute exposure to PM2.5 (mean ± SD, EXP-HF vs FA- HF, 172.8 ± 23.4 vs 156.7 ± 17.6, p <0.05; EXP-RC vs FA-RC, 149.8 ± 19.2, 139.7 ± 15.3, ns; ANOVA). The gene expression profile of E-selectin, IL-6, VCAM-1, ICAM-1 and MMP-9, was differently affected by PM2.5 in heart and lung. Proteins activated by inflammatory stimuli involved in the inhibition of insulin signaling are being investigated.