Melanocortin-4 receptor is required for acute homeostatic responses to increased dietary fat.
In response to moderately increased dietary fat content, melanocortin-4 receptor-null mutant (MC4R-/-) mice exhibit hyperphagia and accelerated weight gain compared to wild-type mice. An increased feed efficiency (weight gain/kcal consumed) argues that mechanisms in addition to hyperphagia are instrumental in causing weight gain. We report two specific defects in coordinating energy expenditure with food intake in MC4R-/- mice. Wild-type mice respond to an increase in the fat content of the diet by rapidly increasing diet-induced thermogenesis and by increasing physical activity, neither of which are observed in MC4R-/- mice. Leptin-deficient and MC3R-/- mice regulate metabolic rate similarly to wild-type mice in this protocol. Melanocortinergic pathways involving MC4-R-regulated neurons, which rapidly respond to signals not requiring changes in leptin, thus seem to be important in regulating metabolic and behavioral responses to dietary fat.
Duke Scholars
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Related Subject Headings
- Weight Gain
- Thermogenesis
- Reference Values
- Receptors, Corticotropin
- Receptor, Melanocortin, Type 4
- Receptor, Melanocortin, Type 3
- Physical Exertion
- Neurology & Neurosurgery
- Mice, Knockout
- Mice, Inbred C57BL
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Weight Gain
- Thermogenesis
- Reference Values
- Receptors, Corticotropin
- Receptor, Melanocortin, Type 4
- Receptor, Melanocortin, Type 3
- Physical Exertion
- Neurology & Neurosurgery
- Mice, Knockout
- Mice, Inbred C57BL