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

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dc.contributor.author Chen, Hui en_US
dc.contributor.author Kent, Stephen en_US
dc.contributor.author Morris, Margaret en_US
dc.contributor.editor en_US
dc.date.accessioned 2010-05-28T09:51:32Z
dc.date.available 2010-05-28T09:51:32Z
dc.date.issued 2006 en_US
dc.identifier 2009002002 en_US
dc.identifier.citation Chen Hui, Kent Stephen, and Morris Margaret 2006, 'Is the CCK2 receptor essential for normal regulation of body weight and adiposity?', Blackwell Publishing Ltd, vol. 24, no. 5, pp. 1427-1433. en_US
dc.identifier.issn 0953-816X en_US
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 en_US
dc.language en_US
dc.publisher Blackwell Publishing Ltd en_US
dc.relation.hasversion Accepted manuscript version
dc.relation.isbasedon http://dx.doi.org/10.1111/j.1460-9568.2006.05016.x en_US
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? en_US
dc.parent European Journal of Neuroscience en_US
dc.journal.volume 24 en_US
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 060100 en_US
dc.personcode 105405 en_US
dc.personcode 0000061687 en_US
dc.personcode 0000059258 en_US
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


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