Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuromedin U (NMU) is known to have potent actions on appetite and energy expenditure. Deletion of the NMU gene in mice leads to an obese phenotype, characterized by hyperphagia and decreased energy expenditure. Conversely, transgenic mice that overexpress proNMU exhibit reduced body weight and fat storage. Here, we show that central administration of NMU or the related peptide neuromedin S (NMS) dose-dependently decreases food intake, increases metabolic rate, and leads to significant weight loss in mice. The effects of NMU and NMS on both feeding and metabolism are almost completely lost in mice lacking the putative CNS receptor for NMU and NMS, NMUr2. However, NMUr2 knockout mice do not exhibit overt differences in body weight or energy expenditure compared with wild-type mice, suggesting that the dramatic phenotype of the NMU gene knockout mouse is not due simply to the loss of NMU/NMUr2 signaling. Putative proteolytic cleavage sites indicate that an additional peptide is produced from the NMU precursor protein, which is extremely well conserved between human, mouse, and rat. Here, we demonstrate that this peptide, proNMU(104-136), has a pronounced effect on energy balance in mice. Specifically, central administration of proNMU(104-136) causes a significant but transient ( approximately 4 h) increase in feeding, yet both food intake and body weight are decreased over the following 24 h. proNMU(104-136) administration also significantly increased metabolic rate. These results suggest that proNMU(104-136) is a novel modulator of energy balance and may contribute to the phenotype exhibited by NMU knockout mice.
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PMID:Appetite-modifying actions of pro-neuromedin U-derived peptides. 1953 38

The recently discovered nesfatin-1 is regulated by hunger and satiety. The precursor protein NUCB2 is proteolytically cleaved into three resulting fragments: nesfatin-1, nesfatin-2, and nesfatin-3. The middle segment of nesfatin-1 (M30) is responsible for limiting food intake, while the exact physiological role of nesfatin-2 and nesfatin-3 are not currently known yet. This hormone plays role/roles on diabetic hyperphagia, epilepsy, mood, stress, sleeping, anxiety, hyperpolarization, depolarization, and reproductive functions. This review will address nesfatin, focusing on its discovery and designation, biochemical structure, scientific evidence of its anorexigenic character, the results of the human and animal studies until the present day, its main biochemical and physiological effects, and its possible clinical applications.
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PMID:Multi-functional peptide hormone NUCB2/nesfatin-1. 2352 35