THE EFFECTS OF SUBCHRONIC CADMIUM EXPOSURE ON INSULIN AND RELATED BLOOD BIOCHEMICAL INDICATORS IN MICE

Shengqing Zhou, Zeling Zhu, Weiliang Zhu, Linda Zhu, Sam Zhang, Qian Lu and Zhiheng Zhou*

ABSTRACT

Background: Cadmium (Cd), as a common environmental pollutant, has been widely proved to be carcinogenic and toxic to multiple organs. However, the mechanism of low-dose and long-term exposure on pancreatic function is still unclear, especially its association with diabetes development needs to be verified by experiments. Objective: This study armed to explore the dose-dependent effects of subchronic cadmium exposure on insulin secretion, glucose metabolism and liver and kidney function in mice, and to provide experimental evidence for the toxic mechanism of cadmium-induced diabetes. Methods: 30 ICR mice were randomly divided into three groups, each group with 10 mice: control group (pure water), low dose group (50 mg/L CdCl₂) and high dose group (200 mg/L CdCl₂). The mice were poisoned by drinking cadmium solution and pure water for 14 weeks, and the body weight, blood routine, urine routine, fasting blood glucose/insulin and liver and kidney function indexes were detected. Results: Compared to the control group, the body weight of the cadmium-exposed mice did not change significantly after 14 weeks of exposure to cadmium. However, the high-dose group showed a decrease in white blood cells (down 12.3%), hemoglobin (down 9.8%), and hematocrit (down 7.5%) (P <0.05). The urinary creatinine levels were significantly higher in the low-dose group (275.80±33.194 μmol/L) and the high-dose group (276.77±27.098 μmol/L) than in the blank control group (223.02±41.678 μmol/L), while the urinary β2-microglobulin levels were notably increased in the high-dose group (6.70±3.054 vs 11.985±6.046ng/mL). Fasting serum insulin levels were significantly lower in the low-dose group (249.76±5.827pg/mL) and the high-dose group (178.32±19.851pg/mL) than in the blank control group (290.24±23.919pg/mL), but there was no significant difference in blood glucose levels among the three groups. Fasting serum alanine aminotransferase and aspartate aminotransferase concentrations were higher in the low-dose and high-dose groups compared to the blank control group, with statistically significant differences (P <0.05), while there were no significant differences in creatinine, urea, or urea/creatinine ratios (P> 0.05). Conclusions: Subchronic cadmium poisoning can inhibit insulin secretion in mice and cause partial liver and kidney damage, suggesting that cadmium pollution may increase the risk of diabetes through multi-organ interaction. This study provides a scientific basis for setting environmental cadmium exposure threshold and prevention and control strategies.

Keywords: Cadmium, mice, insulin, toxicity, liver function.