Abstract:
:Here, we report the isolation and characterization of an endogenous peptide ligand of GPR103 from rat brains. The purified peptide was found to be the 43-residue RF-amide peptide QRFP. We also describe two mouse homologues of human GPR103, termed mouse GPR103A and GPR103B. QRFP binds and activates the human GPR103, as well as mouse GPR103A and GPR103B, with nanomolar affinities in transfected cells. Systematic in situ hybridization analysis in mouse brains showed that QRFP is expressed exclusively in the periventricular and lateral hypothalamus, whereas the two receptor mRNAs are distinctly localized in various brain areas without an overlap to each other. When administered centrally in mice, QRFP induced feeding behavior, accompanied by increased general locomotor activity and metabolic rate. QRFP-induced food intake was abolished by preadministration of BIBP3226, a specific antagonist for the Y1 neuropeptide Y receptor. Hypothalamic prepro-QRFP mRNA expression was up-regulated upon fasting and in genetically obese ob/ob and db/db mice. Central QRFP administration also evoked highly sustained elevation of blood pressure and heart rate. Our findings suggest that QRFP and GPR103A/B may regulate diverse neuroendocrine and behavioral functions and implicate this neuropeptide system in metabolic syndrome.
journal_name
Proc Natl Acad Sci U S Aauthors
Takayasu S,Sakurai T,Iwasaki S,Teranishi H,Yamanaka A,Williams SC,Iguchi H,Kawasawa YI,Ikeda Y,Sakakibara I,Ohno K,Ioka RX,Murakami S,Dohmae N,Xie J,Suda T,Motoike T,Ohuchi T,Yanagisawa M,Sakai Jdoi
10.1073/pnas.0602371103subject
Has Abstractpub_date
2006-05-09 00:00:00pages
7438-43issue
19eissn
0027-8424issn
1091-6490pii
0602371103journal_volume
103pub_type
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