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

Chen, H; Kent, S; Morris, MJ

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

Chen, H

Kent, S Morris, MJ

Permalink

Publication Type:: Journal Article
Citation:: European Journal of Neuroscience, 2006, 24 (5), pp. 1427 - 1433
Issue Date:: 2006-09-01

Closed Access

	Filename	Description	Size
	2009002002.pdf		158.57 kB	Adobe PDF	View/Open

Copyright Clearance Process

Recently Added
In Progress
Closed Access

This item is closed access and not available.

Full metadata record

Field	Value	Language
dc.contributor.author	Chen, H https://orcid.org/0000-0001-6883-3752	en_US
dc.contributor.author	Kent, S	en_US
dc.contributor.author	Morris, MJ	en_US
dc.date.issued	2006-09-01	en_US
dc.identifier.citation	European Journal of Neuroscience, 2006, 24 (5), pp. 1427 - 1433	en_US
dc.identifier.issn	0953-816X	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. © The Authors (2006).	en_US
dc.relation.ispartof	European Journal of Neuroscience	en_US
dc.relation.isbasedon	10.1111/j.1460-9568.2006.05016.x	en_US
dc.subject.classification	Neurology & Neurosurgery	en_US
dc.subject.mesh	Animals	en_US
dc.subject.mesh	Mice, Knockout	en_US
dc.subject.mesh	Mice	en_US
dc.subject.mesh	Body Weight	en_US
dc.subject.mesh	Corticosterone	en_US
dc.subject.mesh	Insulin	en_US
dc.subject.mesh	Leptin	en_US
dc.subject.mesh	Neuropeptide Y	en_US
dc.subject.mesh	Receptor, Cholecystokinin B	en_US
dc.subject.mesh	Radioimmunoassay	en_US
dc.subject.mesh	Sex Factors	en_US
dc.subject.mesh	Brain Chemistry	en_US
dc.subject.mesh	Female	en_US
dc.subject.mesh	Male	en_US
dc.subject.mesh	Adiposity	en_US
dc.title	Is the CCK2 receptor essential for normal regulation of body weight and adiposity?	en_US
dc.type	Journal Article
utslib.citation.volume	5	en_US
utslib.citation.volume	24	en_US
utslib.for	0601 Biochemistry and Cell Biology	en_US
utslib.for	1109 Neurosciences	en_US
utslib.for	1701 Psychology	en_US
utslib.for	1702 Cognitive Sciences	en_US
pubs.embargo.period	Not known	en_US
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 Life Sciences
pubs.organisational-group	/University of Technology Sydney/Strength - CHT - Health Technologies
utslib.copyright.status	closed_access
pubs.issue	5	en_US
pubs.publication-status	Published	en_US
pubs.volume	24	en_US

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. © The Authors (2006).

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/9737