期刊
NEUROBIOLOGY OF DISEASE
卷 44, 期 1, 页码 1-8出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2011.05.006
关键词
Huntington's disease; Weight loss; R6/2 mouse; Enteric nervous system; Gastrointestinal motility; Gut; Diarrhea; Malabsorption
资金
- BenteRexed Foundation
- Swedish Research Council
- Crafoord Foundation
- Royal Physiological Society
- Marie Curie Actions Fellowship [RTN MRTN-CT-2003-504636]
- Netherlands Organization for Scientific Research [017.003.098]
- CHDI Foundation
Weight loss is the most important non-neurological complication of Huntington's disease (HD). It correlates with disease progression and affects the quality of life of HD patients, suggesting that it could be a valuable target for therapeutic intervention. The mechanism underlying weight loss in HD is unknown. Mutant huntingtin, the protein that causes the disease, is not only expressed in the brain, but also along the gastrointestinal (GI) tract. Here we demonstrate that the Cl tract of HD mice is affected. At the anatomical level we observed loss of enteric neuropeptides, as well as decreased mucosal thickness and villus length. Exploring the functions of the Cl system we found impaired gut motility, diarrhea, and malabsorption of food. The degree of malabsorption was inversely associated with body weight, suggesting that GI dysfunction plays an important role in weight loss in HD mice. In summary, these observations suggest that the GI tract is affected in HD mice and that GI dysfunction contributes to nutritional deficiencies and weight loss. (C) 2011 Elsevier Inc. All rights reserved.
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