Endogenous neuromedin U has anorectic effects in the Japanese quail

Abstract

Neuromedin U (NMU), which is a brain-gut peptide, was first isolated as a smooth-muscle-contracting peptide from the porcine spinal cord in 1985. Intracerebroventricular (icv) injection of NMU into rats significantly reduced the food intake during dark period, and increased oxygen consumption, locomotor activity, and body temperature suggested that NMU is an anorectic and catabolic signaling molecule in mammals. In this study, we elucidated the central role of NMU in avian species using Japanese quail. Gene cloning analysis revealed that the amino acid sequence of Japanese quail NMU has high homology with that of chick, and low homology with that of rat except the C-terminal biologically active region. RT-PCR analysis revealed that NMU mRNA was expressed in various central and peripheral tissues. Both intraperitoneal (ip) and icv administration of synthetic Japanese quail NMU resulted in a significant reduction in food intake and increase in body temperature and locomotor activity in Japanese quails. Conversely, the administration of rat NMU into Japanese quail resulted in the opposite effects on food intake, body temperature, and locomotor activity. These opposite results may indicate that rat NMU act as an antagonist toward the Japanese quail NMU receptor. These results suggest that endogenous NMU plays an important role in the regulation of food intake and body temperature in avian species.