Neuromedin U (Nmu) is an evolutionarily conserved neuropeptide. It regulates diverse physiologic effects such as blood pressure, stress responses, metabolic and feeding behavior, pain perception, and neuroendocrine functions. It signals via two G-protein-coupled receptors, NMUR1 and NMUR2 [1,3].

Global loss of Nmu expression in male and female mice leads to high bone mass due to elevated bone formation rate, indicating its role in regulating bone remodeling [3,5]. Nmu/Nms/Gpr176 triple-deficient mice show enhanced light-resetting of circadian locomotor activity, suggesting a mechanism requiring Nmu, Nms, and Gpr176 for proper modulation of light-induced phase shift [2]. Also, high expression of Nmu is associated with poor prognosis in diseases like lung adenocarcinoma, colon cancer, and endometrial cancer, promoting cancer cell progression [4,6,7].

In conclusion, Nmu plays crucial roles in various biological processes including bone remodeling, circadian rhythm regulation, and is involved in disease progression of certain cancers. Gene knockout mouse models, such as the Nmu-deficient mice, have been instrumental in revealing these functions, providing insights into potential therapeutic targets for metabolic, circadian, and cancer-related disorders.