Abstract
Obesity is now a public health concern. The leading cause of obesity is an energy imbalance between ingested and expended calories. The mechanisms of feeding behavior and energy metabolism are regulated by a complex of various kinds of molecules, including anorexigenic and orexigenic neuropeptides. One of these neuropeptides, neuromedin U (NMU), was isolated in the 1980s, and its specific receptors, NMUR1 and NMUR2, were defined in 2000. A series of subsequent studies has revealed many of the physiological roles of the NMU system, including in feeding behavior, energy expenditure, stress responses, circadian rhythmicity, and inflammation. Particularly over the past decades, many reports have indicated that the NMU system plays an essential and direct role in regulating body weight, feeding behavior, energy metabolism, and insulin secretion, which are tightly linked to obesity pathophysiology. Furthermore, another ligand of NMU receptors, NMS (neuromedin S), was identified in 2005. NMS has physiological functions similar to those of NMU. This review summarizes recent observations of the NMU system in relation to the pathophysiology of obesity in both the central nervous systems and the peripheral tissues.
Highlights
Obesity is a global epidemic caused by an imbalance resulting from excessive energy intake and inefficient energy expenditure [1,2]
Feeding behavior and energy homeostasis are regulated in a complex manner by various kinds of appetite-regulating peptides, including orexigenic neuropeptide Y (NPY), agouti-related peptide (AGRP), ghrelin, anorexigenic α-melanocyte-stimulating hormone (α-MSH), corticotropin-releasing hormone (CRH), and cocaine- and amphetamine -regulated transcript (CART) [1,2,3]
This review provides an overview of these novel functions of the Neuromedin U (NMU) system, including homeostatic or hedonic feeding behavior, obesityrelated complications, insulin secretion, and inflammation, and summarizes each function in terms of the molecular aspects and therapeutic possibilities
Summary
Obesity is a global epidemic caused by an imbalance resulting from excessive energy intake and inefficient energy expenditure [1,2]. The NMU system, which includes the NMU-specific receptors, NMUR1 ( known as GPR66/FM-3) and NMUR2 ( called FM-4/TGR-1), which both belong to the. G-protein-coupled receptors (GPCRs), is essential for the contraction of smooth muscles and is involved in feeding behavior, energy expenditure, stress responses, circadian rhythmicity, and inflammation [5,6,7,8,9,10,11,12]. This review provides an overview of these novel functions of the NMU system, including homeostatic or hedonic feeding behavior, obesityrelated complications, insulin secretion, and inflammation, and summarizes each function in terms of the molecular aspects and therapeutic possibilities
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