Proadrenomedullin N‐terminal 20 peptide (PAMP) elevates blood glucose levels via bombesin receptor in mice

FEBS Letters

Wada, Keiji¹  Inui, Akio³  Wada, Estuko¹  Ohinata, Kousaku²  Asakawa, Akihiro³  Yoshikawa, Masaaki² 

[1] Department of Degenerative Neurological Diseases, National Institute of Neuroscience, NCNP 4-1-1 Ogawahigashi, Kodaira, Tokyo 187-8502, Japan;Department of Functional Food Resources, Research Institute for Food Science, Kyoto University, Gokasho Uji, Kyoto 611-0011, Japan;Second Department of Internal Medicine, Kobe University School of Medicine, 7-5-2 Kusunoki-cho, Chuo-ku, Kobe 650-0017, Japan

关键词: Proadrenomedullin N-terminal 20 peptide;    Hyperglycemia;    Bombesin;    Gastrin-releasing peptide preferring receptor;    α-Adrenergic activation;    PAMP;    proadrenomedullin N-terminal 20 peptide;    BN;    bombesin;    GRP-R;    gastrin-releasing peptide preferring receptor;    i.c.v.;    intra-third cerebroventricular;   

DOI  :  10.1016/S0014-5793(00)01529-5

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

We found a potent hyperglycemic effect of proadrenomedullin N-terminal 20 peptide (PAMP) after intra-third cerebroventricular administration at a dose of 10 nmol in fasted mice. PAMP has four homologous residues with bombesin (BN), a hyperglycemic peptide. PAMP showed affinity for gastrin-releasing peptide preferring receptor (GRP-R) and neuromedin B preferring receptor. The PAMP-induced hyperglycemic effect was inhibited by [D-Phe⁶, Leu-NHEt¹³, des-Met¹⁴]-BN (6–14), GRP-R specific antagonist, indicating that the hyperglycemic effect is mediated at least in part via GRP-R. Furthermore, pretreatment of α-adrenergic blocker inhibited the PAMP-induced hyperglycemia and hyperglucagonemia, suggesting that the increase of glucagon secretion through α-adrenergic activation is involved in this hyperglycemic effect of PAMP.

【 授权许可】

Unknown