4.0 Article

Niclosamide as an anti-obesity drug: an experimental study

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SPRINGER
DOI: 10.1007/s40519-017-0373-1

Keywords

Niclosamide; Obesity; Mitochondrial uncoupling; Lipid profile

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Funding

  1. Ministry of Higher Education and Scientific Research in Iraq [998-10]

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Background Niclosamide is a well-known anthelminthic drug that exert its effects at least in part through induction of mitochondrial uncoupling. The cycling of mitochondrial proton plays an essential role in regulation of basal metabolic rate, so modulation of mitochondrial uncoupling may be helpful approach to fight obesity. Objective To assess the anti-obesity effects of niclosamide on mice with induced obesity. Materials and methods Thirty male Albino mice, 8-10 weeks old, were divided randomly and equally in to three groups; Group 1 fed with standard diet, whereas both Groups 2 and 3 were fed with high fat diet (HFD). At 10 weeks, the studied groups continue in the same type of diet as before for another 4 weeks, but additionally both of Group1 and 2 received placebo treatment as normal control and high fat diet control respectively, whereas Group 3 received oral niclosamide (140 mg/kg/day) as treatment group. The anti-obesity effects of niclosamide were evaluated by testing its effects on food intake, bodyweight, glycemic indices, and lipid profile. Result It was found that administration of niclosamide 140 mg/kg/day to HFD fed mice (Group3) for 4 weeks resulted in significant (P < 0.05) decline in the food intake and bodyweight of this group as compared with HFD control. Furthermore, niclosamide also resulted in significant (P < 0.05) lowering of the fasting blood glucose, fasting plasma insulin and improve insulin resistance. Likewise, niclosamide ameliorates the harmful effects of HFD on lipid profile by significant lowering of cholesterol, triglycerides, and LDL (P < 0.05). Conclusion Niclosamide has promising effects as an anti-obesity drug. It not just lowers bodyweight in mice, but, at the same time, it reverses metabolic disturbance induced by obesity.

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