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

Author:
  • Jorien m van der Burg
  • Karl Bacos
  • Nigel I Wood
  • Andreas Lindqvist
  • Nils Wierup
  • Ben Woodman
  • Jaclyn Wamsteeker
  • Ruben Smith
  • Tomas Deierborg
  • Michael J Kuhar
  • Gillian P Bates
  • Hindrik Mulder
  • Charlotte Erlanson-Albertsson
  • Jennifer Morton
  • Patrik Brundin
  • Åsa Petersén
  • Maria Björkqvist
Publishing year: 2008
Language: English
Pages: 41-51
Publication/Series: Neurobiology of Disease
Volume: 29
Issue: 1
Document type: Journal article
Publisher: Elsevier
Additional info: The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Apetite Regulation (013212030), Molecular Metabolism (013212001), Neuronal Survival (013212041), Translational Neuroendocrinology (013210010), Neuroendocrine Cell Biology (013212008)

Abstract english

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.

Keywords

  • Neurosciences

Other

Published
  • Appetite Regulation
  • Translational Neuroendocrinology
  • ISSN: 0969-9961
Karl Bacos
E-mail: karl [dot] bacos [at] med [dot] lu [dot] se

Assistant researcher

Diabetes - Epigenetics

+46 40 39 12 19

91-12-022

Jan Waldenströms gata 35, Malmö

36

Lund University Diabetes Centre, CRC, SUS Malmö, Jan Waldenströms gata 35, House 91:12. SE-214 28 Malmö. Telephone: +46 40 39 10 00