1. Central actions of neuromedin U via corticotropin-releasing hormone.
- Author
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Hanada T, Date Y, Shimbara T, Sakihara S, Murakami N, Hayashi Y, Kanai Y, Suda T, Kangawa K, and Nakazato M
- Subjects
- Animals, Appetite Regulation drug effects, Appetite Regulation physiology, Body Temperature Regulation drug effects, Body Temperature Regulation physiology, Corticotropin-Releasing Hormone deficiency, Homeostasis drug effects, Homeostasis physiology, Hypothalamus drug effects, Hypothalamus physiology, Injections, Intraventricular, Mice, Mice, Inbred C57BL, Mice, Knockout, Oxygen Consumption drug effects, Oxygen Consumption physiology, Corticotropin-Releasing Hormone metabolism, Energy Metabolism drug effects, Energy Metabolism physiology, Feeding Behavior drug effects, Feeding Behavior physiology, Neuropeptides administration & dosage
- Abstract
Neuromedin U (NMU), a hypothalamic peptide, has been known to be involved in feeding behavior as a catabolic signaling molecule. However, little is known about the participation of NMU in the neuronal network. One NMU receptor, NMU2R, is abundantly expressed in the hypothalamic paraventricular nucleus, where corticotrophin-releasing hormone (CRH) is synthesized. The functions of CRH, regulation of stress response and feeding behavior, are comparable with those of NMU. Here, we have investigated the functional relationships between NMU and CRH using CRH knockout (KO) mice. Intracerebroventricular administration of NMU suppressed dark-phase food intake and fasting-induced feeding in wild-type mice. In contrast, these suppressions were not observed in CRH KO mice. NMU-induced increases in oxygen consumption and body temperature were attenuated in CRH KO mice. These results suggest that NMU plays a role in feeding behavior and catabolic functions via CRH. This study demonstrates a novel hypothalamic pathway that links NMU and CRH in the regulation of feeding behavior and energy homeostasis.
- Published
- 2003
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