Is the CCK2 receptor essential for normal regulation of body weight and adiposity?

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dc.contributor.author Chen, H
dc.contributor.author Kent, S
dc.contributor.author Morris, M
dc.date.accessioned 2010-05-28T09:51:32Z
dc.date.issued 2006-01
dc.identifier.citation European Journal of Neuroscience, 2006, 24 (5), pp. 1427 - 1433
dc.identifier.issn 0953-816X
dc.identifier.other C1UNSUBMIT en_US
dc.identifier.uri http://hdl.handle.net/10453/9737
dc.description.abstract Cholecystokinin (CCK) is a gastrointestinal satiety signal released from the duodenum to terminate feeding, via CCK1 receptors. CCK2 receptors are considered to be involved in anxiety. CCK2 receptor knockout mice have increased body weight and food intake. Little is known regarding the effects of CCK2 receptor deficiency on adipose distribution and hypothalamic feeding regulators such as neuropeptide Y (NPY), a powerful stimulator of feeding. Adult (10?week) CCK2 receptor knockout and wild-type mice were anaesthetized and killed by decapitation. Brain sections, organs and fat tissue were dissected. Plasma leptin, insulin and brain NPY content were measured by radioimmunoassay. Female CCK2 receptor knockout mice weighed more than control mice (22.0?±?0.2 vs. 19.9?±?0.4?g, P?<?0.05), with this difference being less marked in male mice (26.4?±?0.4 vs. 25.6?±?0.6?g). Fat masses in all locations sampled were significantly smaller in CCK2 receptor knockout mice of both genders (P?<?0.05), resulting in lower plasma leptin and insulin levels. NPY concentrations were significantly increased in arcuate nucleus and anterior hypothalamus in both male and female CCK2 receptor knockout mice, and total hypothalamic NPY content was increased by 7 and 9% in males and females, respectively (P?<?0.05). CCK2 receptor deletion was associated with increased body weight and hypothalamic NPY content, but reduced fat masses and plasma leptin and insulin. Increased NPY might contribute to increased food intake in CCK2 receptor knockout mice. Further work needs to focus on the metabolic changes
dc.publisher Blackwell Publishing Ltd
dc.relation.hasversion Accepted manuscript version
dc.relation.isbasedon 10.1111/j.1460-9568.2006.05016.x
dc.rights The definitive version is available at www.blackwell-synergy.com
dc.title Is the CCK2 receptor essential for normal regulation of body weight and adiposity?
dc.type Journal Article
dc.parent European Journal of Neuroscience
dc.journal.volume 5
dc.journal.volume 24
dc.journal.number 5 en_US
dc.publocation Oxford, UK en_US
dc.identifier.startpage 1427 en_US
dc.identifier.endpage 1433 en_US
dc.cauo.name SCI.Medical and Molecular Biosciences en_US
dc.conference Verified OK en_US
dc.for 0601 Biochemistry and Cell Biology
dc.personcode 105405
dc.percentage 100 en_US
dc.classification.name Biochemistry and Cell Biology en_US
dc.classification.type FOR-08 en_US
dc.edition en_US
dc.custom en_US
dc.date.activity en_US
dc.location.activity en_US
dc.description.keywords CCK2 receptor knockout mouse; insulin; leptin; neuropeptide Y en_US
dc.description.keywords CCK2 receptor knockout mouse
dc.description.keywords insulin
dc.description.keywords leptin
dc.description.keywords neuropeptide Y
pubs.embargo.period Not known
pubs.organisational-group /University of Technology Sydney
pubs.organisational-group /University of Technology Sydney/Faculty of Science
pubs.organisational-group /University of Technology Sydney/Faculty of Science/School of Medical and Molecular Sciences
pubs.organisational-group /University of Technology Sydney/Strength - Health Technologies
utslib.copyright.status Closed Access
utslib.copyright.date 2015-04-15 12:17:09.805752+10


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