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
| Autor: | Pauline Brendler Goettems-Fiorin, Gabriela Elisa Hirsch, Analú Bender Dos Santos, Marieli Oara Amaral Fagundes da Silva, Matias Nunes Frizzo, Thiago Gomes Heck, Aline Sfalcin Mai, Lílian Corrêa Costa Beber, Mirna Stela Ludwig |
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| Rok vydání: | 2020 |
| Předmět: |
medicine.medical_specialty
Antioxidant Health Toxicology and Mutagenesis medicine.medical_treatment Adipose tissue Inflammation Oxidative phosphorylation 010501 environmental sciences medicine.disease_cause 01 natural sciences Impaired glucose tolerance Internal medicine Heat shock protein medicine Environmental Chemistry Saline 0105 earth and related environmental sciences Chemistry digestive oral and skin physiology nutritional and metabolic diseases food and beverages General Medicine medicine.disease Pollution Endocrinology medicine.symptom Oxidative stress |
| Zdroj: | Environmental Science and Pollution Research. 27:32006-32016 |
| ISSN: | 1614-7499 0944-1344 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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