Journal
NATURE NEUROSCIENCE
Volume 4, Issue 6, Pages 605-611Publisher
NATURE RESEARCH
DOI: 10.1038/88423
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- OAPP OPHS HHS [PPGDK55819] Funding Source: Medline
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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.
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