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Peptide YY , neuropeptide Y and corticotrophin‐releasing factor modulate gastrointestinal motility and food intake during acute stress
Author(s) -
Forbes Sarah C.,
Cox Helen M.
Publication year - 2014
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/nmo.12428
Subject(s) - peptide yy , neuropeptide y receptor , medicine , endocrinology , motility , antagonist , receptor , neuropeptide , receptor antagonist , endogeny , chemistry , biology , genetics
Background Peripheral neuropeptide Y ( NPY ) provides protection against the endocrine, feeding and gastrointestinal ( GI ) responses to stress; however, it is not yet established how it interacts with corticotrophin‐releasing factor ( CRF ) to mediate these effects. Peptide YY ( PYY ) also has significant roles in GI motility and food intake but little is known about its role in stress responses. Methods Upper GI transit, fecal pellet output ( FPO ) and feeding responses, and the role of CRF 1 receptors, during restraint or a novel environment stress, were ascertained in PYY −/−, NPY −/− and wild type ( WT ) mice, with CRF and the CRF 1 antagonist, antalarmin, injected intraperitoneally. Key Results Upper GI transit and FPO were significantly increased in PYY −/− mice during restraint stress. Exogenous CRF increased defecation during placement in a novel environment in WT mice through CRF 1 , while CRF 1 blockade reduced defecation in WT and NPY −/− mice but had no effect in PYY −/− mice. In addition, CRF 1 blockade had no effect on upper GI transit in WT mice, or on food intake in PYY −/− or NPY −/− mice, but it significantly increased food intake in WT mice. Conclusions & Inferences Endogenous NPY appears to inhibit the colonic motor response induced by CRF 1 activation, unlike PYY , while both peptides are required for CRF 1 modulation of feeding behavior during stress. Overall, these results provide new insights into the mechanism by which PYY and NPY affect stress responses.