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Nesfatin‐1 Stimulates Stress Hormone Secretion
Author(s) -
Samson Willis K,
Yosten Gina LC,
Ferguson Alastair V
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb621
Subject(s) - oxytocin , endocrinology , medicine , vasopressin , secretion , neuropeptide , hormone , plasma levels , corticotropin releasing hormone , chemistry , receptor
Cellular actions of nesfatin‐1 on oxytocin (OT), vasopressin (AVP) and corticotropin releasing factor (CRF) neurons (J Neuroendocrinol 20:255,2008), the activation of early gene expression in those types of neurons following stress (Brain Res 1300:114,2009), and the ability of nesfatin‐1 to elicit fear and anxiety behaviors (Psychopharmacol 201:115,2008; AJP 297:R330,2009) suggested a role for nesfatin‐1 in the stress response. In conscious, unrestrained male rats i.c.v. administration of 180 pmole nesfatin‐1 resulted in significant increases in plasma levels of AVP (vehicle: 1.9±0.5, n=8; nesfatin‐1: 10.0±3.4 pg AVP/ml, n=8, p = 0.018) and ACTH (vehicle: 6.0±1.4; nesfatin‐1: 28.5±7.7 pg ACTH/ml; p<0.01) 10 minutes later. Plasma OT levels were unchanged. The actions of nesfatin‐1 on food intake and cardiovascular function are dependent upon activation of POMC neurons (AJP 297:R330,2009) and roles for OT in those actions have been reported. We suggest that nesfatin‐1 activates stress hormone secretion by releasing AVP and CRF but that the ability of nesfatin‐1 to activate OT neurons reflects an action to release OT centrally and not into the peripheral plasma.