Goettems-Fiorin Pauline Brendler, Grochanke Bethânia Salamoni, Baldissera Fernanda Giesel, Dos Santos Analu Bender, Homem de Bittencourt Paulo Ivo, Ludwig Mirna Stela, Rhoden Claudia Ramos, Heck Thiago Gomes
Research Group in Physiology, Department of Life Sciences, Regional University of Northwestern Rio Grande do Sul State (UNIJUI), Rua do Comércio, 3000 - Bairro Universitário, Ijuí, RS, Brazil.
Laboratory of Oxidative Stress and Air Pollution, Postgraduate Program in Health Sciences, Federal University of Health Sciences of Porto Alegre (UFCSPA), Porto Alegre, RS, Brazil.
J Physiol Biochem. 2016 Dec;72(4):643-656. doi: 10.1007/s13105-016-0503-7. Epub 2016 Jun 29.
Exposure to fine particulate matter (PM) air pollution is a risk factor for type 2 diabetes (T2DM). We argue whether the potentiating effect of PM over the development of T2DM in high-fat diet (HFD)-fed mice would be related to modification in cell stress response, particularly in antioxidant defenses and 70-kDa heat shock proteins (HSP70) status. Male mice were fed standard chow or HFD for 12 weeks and then randomly exposed to daily nasotropic instillation of PM for additional 12 weeks under the same diet schedule, divided into four groups (n = 14-15 each): Control, PM, HFD, and HFD + PM were evaluated biometric and metabolic profiles of mice, and cellular stress response (antioxidant defense and HSP70 status) of metabolic tissues. Extracellular to intracellular HSP70 ratio ([eHSP72]/[iHSP70]), viz. H-index, was then calculated. HFD + PM mice presented a positive correlation between adiposity, increased body weight and glucose intolerance, and increased glucose and triacylglycerol plasma levels. Pancreas exhibited lower iHSP70 expression, accompanied by 3.7-fold increase in the plasma to pancreas [eHSP72]/[iHSP70] ratio. Exposure to PM markedly potentiated metabolic dysfunction in HFD-treated mice and promoted relevant alteration in cell stress response assessed by [eHSP72]/[iHSP70], a relevant biomarker of chronic low-grade inflammatory state and T2DM risk.
暴露于细颗粒物（PM）空气污染是2型糖尿病（T2DM）的一个风险因素。我们探讨了在高脂饮食（HFD）喂养的小鼠中，PM对T2DM发生发展的增强作用是否与细胞应激反应的改变有关，特别是抗氧化防御和70 kDa热休克蛋白（HSP70）状态的改变。雄性小鼠喂食标准饲料或HFD 12周，然后在相同的饮食方案下，随机每天经鼻滴注PM，持续12周，分为四组（每组n = 14 - 15）：对照组、PM组、HFD组和HFD + PM组，评估小鼠的生物特征和代谢概况，以及代谢组织的细胞应激反应（抗氧化防御和HSP70状态）。然后计算细胞外与细胞内HSP70比值（[eHSP72]/[iHSP70]），即H指数。HFD + PM组小鼠的肥胖、体重增加和葡萄糖不耐受与血糖和血浆三酰甘油水平升高呈正相关。胰腺中iHSP70表达较低，同时血浆与胰腺的[eHSP72]/[iHSP70]比值增加3.7倍。暴露于PM显著增强了HFD处理小鼠的代谢功能障碍，并促进了通过[eHSP72]/[iHSP70]评估的细胞应激反应的相关改变，[eHSP72]/[iHSP7-0]是慢性低度炎症状态和T2DM风险的一个相关生物标志物。
