Neuromedin U--a new target in obesity

With the increasing prevalence of obesity, effective therapies are urgently required. When neuromedin U was administered intracerebroventricularly to rats there was a marked decrease in weight, whereas injection of an antibody to neuromedin U increased food intake. Unlike wild type, Nmu(-/-) mice become obese when freely fed ordinary mouse chow. The plasma levels of insulin, leptin, total cholesterol, triglycerides and free fatty acids were higher in the Nmu(-/-) than wild-type mice. Energy expenditure was lower in Nmu(-/-) mice. The anorexigenic effect of neuromedin U was independent of the leptin signalling pathway. Transgenic mice overexpressing neuromedin U have lower body weight, less somatic and liver fat, were hypophagic, and had improved insulin sensitivity. These data establish neuromedin U as a target in obesity.