The association of subchronic exposure to low concentration of PM2.5 and high-fat diet potentiates glucose intolerance development, by impairing adipose tissue antioxidant defense and eHSP72 levels
2020
Costa Beber, Lílian Corrêa | da Silva, Marieli Oara Amaral Fagundes | dos Santos, Analú Bender | Mai, Aline Sfalcin | Goettems-Fiorin, Pauline Brendler | Frizzo, Matias Nunes | Hirsch, Gabriela Elisa | Ludwig, Mirna Stela | Heck, Thiago Gomes
The subchronic exposure to fine particulate matter (PM₂.₅) and high-fat diet (HFD) consumption lead to glucose intolerance by different mechanisms involving oxidative stress and inflammation. Under stressful conditions, the cells exert a heat shock response (HSR), by releasing the 72-kDa heat shock proteins (eHSP72), fundamental chaperones. The depletion of the HSR can exacerbate the chronic inflammation. However, there are few studies about the early effects of the association of HFD consumption and exposure to low concentrations of PM₂.₅ in the oxidative stress and HSR, in the genesis of glucose intolerance. Thus, we divided 23 male B6129SF2/J mice into control (n = 6), polluted (n = 6), HFD (n = 6), and high-fat diet + polluted (HFD + polluted) (n = 5) groups. Control and polluted received a standard diet (11.4% of fats), while HFD and HFD + polluted received HFD (58.3% of fats). Simultaneously, polluted and HFD + polluted received 5 μg/10 μL of PM₂.₅, daily, 7×/week, while control and HFD were exposed to 10 μL of saline solution 0.9% for 12 weeks. At the 12th week, animals were euthanized. We collected the metabolic tissues to analyze oxidative parameters, total blood to the hematological parameters, and plasma to eHSP72 measurement. The association of HFD and PM₂.₅ impaired glucose tolerance in the 12th week. Besides, it triggered an antioxidant defense by the adipose tissue, which was negatively correlated with eHSP72 levels. In conclusion, a low concentration of PM₂.₅ exposure associated with HFD consumption leads to glucose intolerance, by impairing adipose tissue antioxidant defense and systemic eHSP72 levels.
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