Abstract
Prolactin-releasing peptide (PrRP) is a peptide ligand for the human orphan G-protein-coupled receptor hGR3/GPR10 and causes the secretion of prolactin from anterior pituitary cells1. However, the lack of immunoreactive staining for PrRP in the external layer of the median eminence seems to rule out this peptide as a classical hypophysiotropic hormone2,3,4 and, furthermore, PrRP is less effective than another inducer of prolactin secretion, thyrotropin-releasing hormone, both in vitro and in vivo5,6,7. Here we show a reduction in the expression of PrRP mRNA during lactation and fasting and an acute effect of PrRP on food intake and body weight, supporting the hypothesis of an alternative role for the peptide.
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Acknowledgements
We acknowledge the support of the Biotechnology and Biosciences Research Council and AstraZeneca plc. We also thank N. Rothwell and A. Turnbull for commenting on the manuscript and A. Hardwick for technical assistance.
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Lawrence, C., Celsi, F., Brennand, J. et al. Alternative role for prolactin-releasing peptide in the regulation of food intake. Nat Neurosci 3, 645–646 (2000). https://doi.org/10.1038/76597
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DOI: https://doi.org/10.1038/76597
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