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1 Department of Metabolic Medicine, Imperial College London, London, United Kingdom
* To whom correspondence should be addressed. E-mail: s.bloom{at}imperial.ac.uk.
Intracerebroventricular administration of Neuromedin U (NMU), a hypothalamic neuropeptide, or leptin, an adipostat hormone released from adipose tissue, reduces food intake and increases energy expenditure. Leptin stimulates the release of NMU in vitro and NMU expression is reduced in models of low or absent leptin. We investigated the role of NMU in mediating leptin induced satiety. Intracerebroventricular administration of anti-NMU immunoglobulin (IgG) (5 nmol) to satiated rats significantly increased food intake 4 hours post injection, an effect seen for up to 8 hours post injection. Intracerebroventricular administration of NMU (1 nmol) to fasted rats reduced food intake 1 hour post injection compared to control, an effect attenuated by pre-treatment with anti-NMU IgG. Intracerebroventricular administration of leptin (0.625 nmol) reduced 24 hour food intake. This was partially attenuated by the administration of anti-NMU IgG [24 h post onset of dark phase: vehicle, 22.5 ± 2.0 g; leptin, 13.7 ± 2.3 g (p < 0.005 vs. vehicle), leptin / anti-NMU IgG, 19.4 ± 1.3 g (p < 0.05 vs. leptin)]. Intraperitoneal administration of leptin (1.1 mg / kg bodyweight) reduced 24 hour food intake. This was partially attenuated by ICV administration of anti-NMU IgG [24 h post onset of dark phase: vehicle, 31.4 ± 4.9 g; leptin, 20.8 ± 2.6 g (p < 0.01 vs. vehicle), leptin / anti-NMU IgG, 28.7 ± 1.1 g (p < 0.01 vs. leptin)]. These results suggest that NMU plays a physiological role in the regulation of appetite and partially mediates leptin induced anorexia.
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