Nicotine enhances insulin sensitivity in rats / 第二军医大学学报

ABSTRACT

Objective: To investigate the effect of nicotine on insulin sensitivity in rats and its relationship with PPAR-γ. Methods: Male Sprague-Dawley rats (10-11 weeks old) were randomly divided into saline group and nicotine group, and the two groups were further divided into 3 subgroups 1 week, 3 weeks, and 6 weeks subgroups according to the time they were treated by different agents. Rats were subcutaneously injected with saline (saline group) daily or nicotine (3 mg·kg-1·d-1, nicotine group) for 1 week, 3 weeks, and 6 weeks. The body weights of animals were recorded on a weekly basis. Insulin tolerance tests were performed at 3 weeks and 6 weeks after treatment, and the serum parameters were determined at 1 week, 3 weeks, and 6 weeks after drug administration. At the end of the experiment, fat tissue weights of different body parts were weighed, and PPAR-γ expression in the subcutaneous fat and visceral fat was detected by Western blotting analysis. Results: The body weight increase of rats was inhibited after nicotine treatment. Insulin sensitivity of rats was significantly enhanced 3 weeks and 6 weeks after nicotine treatment (P<0.05), serum triglyceride level was decreased significantly at 3 weeks after nicotine treatment (P<0.01), insulin sensitivity indices were increased after 6 weeks (P<0.05), and both the weight and relative weight of subcutaneous and visceral fat tissues were significantly decreased 6 weeks after nicotine treatment (P<0.01), with the visceral fat decreased more severely than that of the subcutaneous fat. PPAR-γ expressions in the subcutaneous fat and visceral fat tissues were not significantly different between saline and nicotine treated groups. Conclusion: Nicotine can improve insulin sensitivity in rats, which is partly due to the fact that nicotine can decrease the serum triglyceride levels and fat tissue, especially the visceral fat tissue, but has no relation with PPAR-γ protein expression in fat tissue.