Journal
MOLECULAR METABOLISM
Volume 1, Issue 1-2, Pages 86-93Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.molmet.2012.07.003
Keywords
Dopamine; Leptin; Melanocortin system; Hypothalamus; Mesolimbic dopamine system; Food intake
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Funding
- US National Institute of Health [RR01163, DK62202]
- National Health and Medical Research Foundation of Australia
- National Heart Foundation of Australia
- Pfizer Australia
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Food intake is generally accepted to be regulated by the melanocortin system, however recent data suggests that mesolimbic dopaminergic neurons also influence food intake. Whether dopamine signaling is crucial for the acute effect of leptin on feeding is unknown. Using pharmacological and genetic strategies, we tested the hypothesis that the acute inhibitory effect of leptin on food intake is partially mediated by dopamine. Dopamine D2 but not D1 receptor blockade attenuated the acute hypophagic effect of leptin in fasted mice. Additionally, mice lacking the D2R (D2R KO) exhibited an attenuated response to leptin. Conversely, dopamine receptor blockade had no effect on the acute hypophagic effect of melanocortin stimulation or the hyperphagic effect of ghrelin. These findings suggest that dopaminergic pathways do not constitute a normal part of melanocortin-dependent feeding regulation and that the dopaminergic neurocircuitry typically associated with regulation of hedonic feeding likely contributes to feeding regulation by leptin. (C) 2012 Elsevier GmbH. Open access CC-NC-ND license.
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