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

Publisher:
Blackwell Publishing Ltd
Publication Type:
Journal Article
Citation:
European Journal of Neuroscience, 2006, 24 (5), pp. 1427 - 1433
Issue Date:
2006-01
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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?
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