Abstract
CCK octapeptide (CCK-8) is released by the gut in response to a meal and acts via CCK(A) receptors on vagal afferents to induce satiety. However, the central neural pathways by which peripheral CCK-8 affects feeding are poorly understood. In the present study, we tested the hypothesis that norepinephrine (NE) is necessary for satiety induced by peripheral CCK-8 by using mice lacking dopamine beta-hydroxylase (Dbh(-/-)), the enzyme responsible for synthesizing NE and epinephrine from dopamine. We found that Dbh(-/-) mice are as responsive to the satiating effects of CCK-8 as their normal littermates.
MeSH terms
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Animals
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Cholecystokinin / pharmacology*
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Dopamine beta-Hydroxylase / genetics
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Dopamine beta-Hydroxylase / metabolism
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Dose-Response Relationship, Drug
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Feeding Behavior / drug effects*
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Feeding Behavior / physiology
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Female
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Food Deprivation
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Gene Deletion
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Male
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Mice
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Mice, Knockout
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Norepinephrine / biosynthesis
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Norepinephrine / metabolism*
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Peptide Fragments / pharmacology*
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Satiety Response / drug effects*
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Satiety Response / physiology*
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Weight Gain / drug effects
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Weight Gain / physiology
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Weight Loss / drug effects
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Weight Loss / physiology
Substances
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Peptide Fragments
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cholecystokinin 8
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Cholecystokinin
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Dopamine beta-Hydroxylase
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Norepinephrine