Recent studies have shown an intriguing association between air pollution and diabetic risk. This study was to investigate the impact of fine particulate matter (PM2.5) on glucose consequences and pancreas glucose transporter2 (GLUT2) expression in a gestational diabetes mellitus (GDM) rat model. GDM rats were exposed to a low PM2.5 dose during pregnancy. After exposure, interleukin-6 (IL-6) and blood routine tests (BRT) were detected. Pancreas underwent pathologic examination. The levels of pancreatic homogenate glutathione peroxidase (GSH-Px), methane dicarboxylic aldehyde (MDA) and GLUT2 were detected. There were lower maternal body weight gain and fetal weight in the PM2.5 group. Exposure to PM2.5 caused increased absorbed blastocyst number, higher blood mono-nuclear cells (PBMC), platelets and IL-6 levels. The postprandial blood glucose (PBG) was elevated at most time points after exposure. The pancreas of PM2.5 exposed rats revealed periductal inflammation under pathological examination. The pancreatic GSH-Px significantly reduced and MDA increased in exposed group. The pancreatic GLUT2 expression was decreased after PM2.5 exposure. Our study provides direct evidence that PM2.5 exposure can result in pancreatic pathological changes and glycemic consequences in GDM rats. The oxidative response and inflammation are involved in PM2.5 increased risk of pancreatic impairment and glycemic consequences.

Recent studies have shown an association between air pollution and diabetic risk. This study was to investigate the impact of fine particulate matter (PM_2.5) on glucose consequences and pancreas glucose transporter 2 (GLUT2) expression and its related mechanisms in a gestational diabetes mellitus (GDM) rat model. GDM rats were exposed to a low PM_2.5 dose while the controls received saline. Interleukin-6 (IL-6) and blood routine tests (BRT) were detected for analyzing coagulation and inflammation. Pancreas tissues underwent pathologic examination, the levels of homogenate glutathione peroxidase (GSH-Px), and methane dicarboxylic aldehyde (MDA) were detected for oxidative stress estimation, and the degree of GLUT2 expression of pancreas was analyzed. There were lower maternal body weight gain and fetal weight in the PM_2.5 group. Exposure to PM_2.5 caused increased absorbed blastocyst number and postprandial blood glucose (PBG) blood mono-nuclear cells (PBMC), platelets, and IL-6 levels. The pancreas of PM_2.5 exposed rats revealed inflammation under pathological examination. The pancreatic GSH-Px significantly reduced and MDA increased and GLUT2 protein expression decreased after exposure. Our study provides direct evidence that PM_2.5 exposure can result in glycemic consequences in GDM rats. The oxidative response and inflammation are involved in PM_2.5 increased risk of adverse maternal and fetal consequences.