The effects of aluminum (Al) exposure on glucose metabolism and its mechanism were investigated. A total of 30 healthy Wistar male rats were randomly divided into two groups: control (GC) and experimental (GE). The GC group received intraperitoneal normal saline. The GE was established by intraperitoneal injected AlCl3 solution at 10 mg/kg for 30 days. Fasting blood glucose (FBG) and serum levels of insulin (FINS) were measured. The insulin resistance index (HOMA-IR) and pancreatic β cell function index (HOMA-β) were calculated and analyzed with homeostasis model assessment (HOMA). Pancreatic tissue was taken for pathological examination. Glucose transporter 4 (GLUT4) expression in skeletal muscle was detected by quantitative PCR and Western blot. Levels of FBG and HOMA-IR in GE were higher than those in GC at day 10 and 20 (P < 0.05). FINS in GE were higher than those in GC at day 10 and 20, and lower than those in GC at day 30 (P < 0.05). HOMA-β in GE was lower than that of GC at every time point (P < 0.05). Pathology showed that pancreatic damage changed more profoundly with prolongation of time in GE. Expression levels of GLUT4 mRNA and protein in rat skeletal muscle in GE were significantly lower than those in GC (P < 0.05). The results suggested that Al exposure affected glucose metabolism through pancreatic damage and reduction of GLUT4 expression.
Keywords: Aluminum exposure; Glucose transporter 4; Insulin resistance.