Nicotine induces uncoupling protein 1 in white adipose tissue of obese mice

OBJECTIVE: To test the hypothesis that nicotine not only activates uncoupli ng protein1 (UCP1) in brown adipose tissue (BAT), but also induces UCP1 in white adipose tissue (WAT), which contributes to the mitigation of obesity in obese mice. DESIGN: Weights of the whole body, the gastrocnemius muscle, interscapular BAT and subcutaneous and retroperitoneal WAT, food intake and the mRNA and protein of UCP1 in these tissues were measured and immunohistochemistry usi ng antiserum against UCP1 was also performed in obese yellow KK mice treate d with nicotine for 6 months and control mice treated with physiological sa line. RESULTS: Obese mice treated with nicotine for 6 months, compared with those injected with saline, weighed significantly less (P < 0.01) and had smalle r subcutaneous and retroperitoneal WAT pads (P < 0.01), while obese mice th at received nicotine ate less (P < 0.05) than those injected with saline. I n mice treated with nicotine, the mRNA and protein of UCP1 was detected not only in BAT, but also in subcutaneous and retroperitoneal WATs. Immunohist ochemically, the BAT of obese mice contained large lipid droplets and appea red rather WAT-like, but changed to typical brown adipocytes after nicotine treatment. The fat pads of nicotine-treated mice contained many multilocul ar cells that were positive for UCP1. CONCLUSION: Nicotine not only activates UCP1 in BAT, but also induces UCP1 in WAT and decreases food intake, which contributes to the mitigation of ob esity.