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Melanocortin-4 receptor is required for acute homeostatic responses to increased dietary fat

Academic Article
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Overview

authors

  • Butler, Andrew
  • Marks, D. L.
  • Fan, W.
  • Kuhn, C. M.
  • Bartolome, M.
  • Cone, R. D.

publication date

  • June 2001

journal

  • Nature Neuroscience  Journal

abstract

  • 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.

subject areas

  • Adipose Tissue, Brown
  • Animals
  • Crosses, Genetic
  • Dietary Fats
  • Energy Metabolism
  • Feeding Behavior
  • Female
  • Homeostasis
  • Hyperphagia
  • Leptin
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Physical Exertion
  • Receptor, Melanocortin, Type 3
  • Receptor, Melanocortin, Type 4
  • Receptors, Corticotropin
  • Reference Values
  • Thermogenesis
  • Weight Gain
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Identity

International Standard Serial Number (ISSN)

  • 1097-6256

Digital Object Identifier (DOI)

  • 10.1038/88423

PubMed ID

  • 11369941
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Additional Document Info

start page

  • 605

end page

  • 611

volume

  • 4

issue

  • 6

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