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Therapeutic potential of flurbiprofen against obesity in mice

•Flurbiprofen ameliorated obesity in mice after the onset of obesity.•Flurbiprofen did not affect growth.•Flurbiprofen reduced circulating leptin levels in obesity.•It may have therapeutic potency against obesity by ameliorating leptin resistance. Obesity is associated with several diseases includin...

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Published in:Biochemical and biophysical research communications 2014-06, Vol.449 (1), p.132-134
Main Authors: Hosoi, Toru, Baba, Sachiko, Ozawa, Koichiro
Format: Article
Language:English
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Summary:•Flurbiprofen ameliorated obesity in mice after the onset of obesity.•Flurbiprofen did not affect growth.•Flurbiprofen reduced circulating leptin levels in obesity.•It may have therapeutic potency against obesity by ameliorating leptin resistance. Obesity is associated with several diseases including diabetes, nonalcoholic steatohepatitis (NASH), hypertension, cardiovascular disease, and cancer. Therefore, anti-obesity drugs have the potential to prevent these diseases. In the present study, we demonstrated that flurbiprofen, a nonsteroidal anti-inflammatory drug (NSAID), exhibited therapeutic potency against obesity. Mice were fed a high-fat diet (HFD) for 6months, followed by a normal-chow diet (NCD). The flurbiprofen treatment simultaneously administered. Although body weight was significantly decreased in flurbiprofen-treated mice, growth was not affected. Flurbiprofen also reduced the HFD-induced accumulation of visceral fat. Leptin resistance, which is characterized by insensitivity to the anti-obesity hormone leptin, is known to be involved in the development of obesity. We found that one of the possible mechanisms underlying the anti-obesity effects of flurbiprofen may have been mediated through the attenuation of leptin resistance, because the high circulating levels of leptin in HFD-fed mice were decreased in flurbiprofen-treated mice. Therefore, flurbiprofen may exhibit therapeutic potential against obesity by reducing leptin resistance.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2014.04.159