Neurobiology of Disease (Jan 2008)

Increased metabolism in the R6/2 mouse model of Huntington’s disease

  • Jorien M.M. van der Burg,
  • Karl Bacos,
  • Nigel I. Wood,
  • Andreas Lindqvist,
  • Nils Wierup,
  • Ben Woodman,
  • Jaclyn I. Wamsteeker,
  • Ruben Smith,
  • Tomas Deierborg,
  • Michael J. Kuhar,
  • Gillian P. Bates,
  • Hindrik Mulder,
  • Charlotte Erlanson-Albertsson,
  • A. Jennifer Morton,
  • Patrik Brundin,
  • Åsa Petersén,
  • Maria Björkqvist

Journal volume & issue
Vol. 29, no. 1
pp. 41 – 51

Abstract

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Huntington’s disease (HD) is a hereditary disorder characterized by personality changes, chorea, dementia and weight loss. The cause of this weight loss is unknown. The aim of this study was to examine body weight changes and weight-regulating factors in HD using the R6/2 mouse model as a tool. We found that R6/2 mice started losing weight at 9 weeks of age. Total locomotor activity was unaltered and caloric intake was not decreased until 11 weeks of age, which led us to hypothesize that increased metabolism might underlie the weight loss. Indeed, oxygen consumption in R6/2 mice was elevated from 6 weeks of age, indicative of an increased metabolism. Several organ systems that regulate weight and metabolism, including the hypothalamus, the stomach and adipose tissue displayed abnormalities in R6/2 mice. Together, these data demonstrate that weight loss in R6/2 mice is associated with increased metabolism and changes in several weight-regulating factors.

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