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Roles of Corticotropin-Releasing Factor, Neuropeptide Y and Corticosterone in the Regulation of Food Intake In Xenopus laevis

dc.contributor.authorCrespi, Erica J.en_US
dc.contributor.authorVaudry, Huberten_US
dc.contributor.authorDenver, Robert Johnen_US
dc.date.accessioned2010-06-01T18:15:46Z
dc.date.available2010-06-01T18:15:46Z
dc.date.issued2004-03en_US
dc.identifier.citationCrespi, E. J.; Vaudry, H.; Denver, R. J. (2004). "Roles of Corticotropin-Releasing Factor, Neuropeptide Y and Corticosterone in the Regulation of Food Intake In Xenopus laevis ." Journal of Neuroendocrinology 16(3): 279-288. <http://hdl.handle.net/2027.42/71473>en_US
dc.identifier.issn0953-8194en_US
dc.identifier.issn1365-2826en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/71473
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=15049859&dopt=citationen_US
dc.description.abstractIn mammals, hypothalamic control of food intake involves counterregulation of appetite by anorexigenic peptides such as corticotropin-releasing factor (CRF), and orexigenic peptides such as neuropeptide Y (NPY). Glucocorticoids also stimulate food intake by inhibiting CRF while facilitating NPY actions. To gain a better understanding of the diversity and evolution of neuroendocrine feeding controls in vertebrates, we analysed the effects of CRF, NPY and glucocorticoids on food intake in juvenile Xenopus laevis . We also analysed brain CRF and NPY mRNA content and plasma corticosterone concentrations in relation to nutritional state. Intracerebroventricular (i.c.v.) injection of ovine CRF suppressed food intake while CRF receptor antagonist αhelical CRF(9–41) significantly increased food intake relative to uninjected and placebo controls. By contrast, i.c.v. injection of frog NPY and short-term corticosterone treatment increased food intake. Semi-quantitative reverse transcription-polymerase chain reaction analyses showed that CRF and NPY mRNA fluctuated with food intake in the brain region containing the mid-posterior hypothalamus, pretectum, and optic tectum: CRF mRNA decreased 6 h after a meal and remained low through 31 days of food deprivation; NPY mRNA content also decreased 6 h after a meal, but increased to prefeeding levels by 24 h. Plasma corticosterone concentration increased 6 h after a meal, returned to prefeeding levels by 24 h, and did not change with prolonged food deprivation. This postprandial increase in plasma corticosterone may be related to the subsequent increase in plasma glucose and body water content that occurs 24 h postfeeding. Overall, our data support the conclusion that, similar to other vertebrates, CRF is anorexigenic while NPY is orexigenic in X. laevis , and CRF secretion modulates food intake in the absence of stress by exerting an inhibitory tone on appetite. Furthermore, the stress axis is activated in response to food intake, but in contrast to mammals and birds is not activated during periods of food deprivation.en_US
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dc.format.mimetypeapplication/pdf
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dc.publisherBlackwell Science Ltden_US
dc.rights© 2004 Blackwell Publishing Ltden_US
dc.subject.otherCorticotropin-releasing Factoren_US
dc.subject.otherNeuropeptide Yen_US
dc.subject.otherCorticosteroneen_US
dc.subject.otherFeeding Behaviouren_US
dc.subject.otherAmphibiansen_US
dc.titleRoles of Corticotropin-Releasing Factor, Neuropeptide Y and Corticosterone in the Regulation of Food Intake In Xenopus laevisen_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Molecular, Cellular, and Developmental Biology, University of Michigan, Ann Arbor, MI, USA.en_US
dc.contributor.affiliationother† European Institute of Peptide Research, Cellular and Molecular Neuroendocrinology, IFRMP 23, University of Rouen, Mont St Aignan, France.en_US
dc.identifier.pmid15049859en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/71473/1/j.0953-8194.2004.01168.x.pdf
dc.identifier.doi10.1111/j.0953-8194.2004.01168.xen_US
dc.identifier.sourceJournal of Neuroendocrinologyen_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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