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

van der Burg, Jorien m LU ; Bacos, Karl LU orcid ; Wood, Nigel I ; Lindqvist, Andreas LU ; Wierup, Nils LU ; Woodman, Ben ; Wamsteeker, Jaclyn LU ; Smith, Ruben LU ; Deierborg, Tomas LU and Kuhar, Michael J , et al. (2008) In Neurobiology of Disease 29(1). p.41-51
Abstract
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... (More)
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. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Neurobiology of Disease
volume
29
issue
1
pages
41 - 51
publisher
Elsevier
external identifiers
  • wos:000251814700005
  • scopus:36549050391
ISSN
0969-9961
DOI
10.1016/j.nbd.2007.07.029
language
English
LU publication?
yes
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)
id
07e06434-6ba0-4092-9f13-6570de5756d3 (old id 608729)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17920283&dopt=Abstract
date added to LUP
2016-04-01 12:10:50
date last changed
2023-09-01 22:20:37
@article{07e06434-6ba0-4092-9f13-6570de5756d3,
  abstract     = {{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.}},
  author       = {{van der Burg, Jorien m and Bacos, Karl and Wood, Nigel I and Lindqvist, Andreas and Wierup, Nils and Woodman, Ben and Wamsteeker, Jaclyn and Smith, Ruben and Deierborg, Tomas and Kuhar, Michael J and Bates, Gillian P and Mulder, Hindrik and Erlanson-Albertsson, Charlotte and Morton, Jennifer and Brundin, Patrik and Petersén, Åsa and Björkqvist, Maria}},
  issn         = {{0969-9961}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{41--51}},
  publisher    = {{Elsevier}},
  series       = {{Neurobiology of Disease}},
  title        = {{Increased metabolism in the R6/2 mouse model of Huntington's disease.}},
  url          = {{http://dx.doi.org/10.1016/j.nbd.2007.07.029}},
  doi          = {{10.1016/j.nbd.2007.07.029}},
  volume       = {{29}},
  year         = {{2008}},
}