期刊
NEUROGASTROENTEROLOGY AND MOTILITY
卷 26, 期 11, 页码 1605-1614出版社
WILEY
DOI: 10.1111/nmo.12428
关键词
acute stress; corticotrophin-releasing factor; food intake; gastrointestinal and colonic function; neuropeptide Y; peptide YY
资金
- Capacity Building Award in Integrative Mammalian Biology - BBSRC
- BPS
- HEFCE
- KTN
- MRC
- SFC
- Biotechnology and Biological Sciences Research Council [BB/E527098/1] Funding Source: researchfish
- BBSRC [BB/E527098/1] Funding Source: UKRI
BackgroundPeripheral 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. MethodsUpper GI transit, fecal pellet output (FPO) and feeding responses, and the role of CRF1 receptors, during restraint or a novel environment stress, were ascertained in PYY-/-, NPY-/- and wild type (WT) mice, with CRF and the CRF1 antagonist, antalarmin, injected intraperitoneally. Key ResultsUpper 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 CRF1, while CRF1 blockade reduced defecation in WT and NPY-/- mice but had no effect in PYY-/- mice. In addition, CRF1 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 & InferencesEndogenous NPY appears to inhibit the colonic motor response induced by CRF1 activation, unlike PYY, while both peptides are required for CRF1 modulation of feeding behavior during stress. Overall, these results provide new insights into the mechanism by which PYY and NPY affect stress responses.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据