PM2.5 promotes β cell damage by increasing inflammatory factors in mice with streptozotocin.

Abstract

Emerging evidence indicates that exposure to fine particulate matter contributes to the onset of diabetes. The present study aimed to investigate the mechanism of particulate matters (PM)2.5 affecting glucose homeostasis in mice with type 1 diabetes mellitus. Male C57BL/6 mice were housed under filtered air (FA) or PM2.5 for 12 weeks and then received intraperitoneal injection of streptozotocin (STZ; 40 mg/kg) or acetic buffer daily for 5 days. At 4 weeks after the last injection, fasting glucose was tested. In the plasma and liver, cholesterol levels were determined by cholesterol oxidase-peroxidase and triglyceride levels were determined by triglycerophosphate oxidase-peroxidase. Homeostasis model assessment of β cell function (Homa-β) was computed based on fasting insulin and glucose levels. Interleukin-1β (IL-1β) and tumor necrosis factor-α (TNFα) levels in plasma, visceral adipose tissues, RAW264.7 macrophages and MIN6 pancreatic β cells treated with PM2.5 (0-50 µg/ml) were quantified via ELISA. Before STZ injection, fasting blood glucose (FBG) levels were similar between FA and PM2.5 groups. After STZ injection, FBG levels were higher in mice pre-exposed to PM2.5 compared with those pre-exposed to FA. When taking FBG levels ≥7 mmol/l as the criteria for impaired glucose level, its incidence was 53.3% and 77.8% in FA and PM2.5 groups, respectively. Independent of STZ injection, IL-1β levels in the adipose tissue were upregulated in mice pre-exposed to PM2.5 compared with FA. The addition of PM2.5 stimulated IL-1β and TNFα production in macrophages and pancreatic β cells, and inhibited the secretion of insulin from MIN6 cells in a dose-dependent manner. In conclusion, pre-exposure of PM2.5 impaired pancreatic β cells in mice upon STZ injection, partially via enhanced inflammation, and suppressed the secretion of insulin.