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Deficient Rab11 activity underlies glucose hypometabolism in primary neurons of Huntington’s disease mice

Li, Xueyi, Valencia, Antonio, McClory, Hollis, Sapp, Ellen, Kegel, Kimberly B., DiFiglia, Marian·2012·Biochemical and Biophysical Research Communications
DOI 10.1016/j.bbrc.2012.04.070
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Abstract

Huntington's disease (HD) is a progressive neurodegenerative disorder caused by a CAG repeat expansion in the huntingtin gene. Positron emission tomography studies have revealed a decline in glucose metabolism in the brain of patients with HD by a mechanism that has not been established. We examined glucose utilization in embryonic primary cortical neurons of wild-type (WT) and HD knock-in mice, which have 140 CAG repeats inserted in the endogenous mouse huntingtin gene (HD(140Q/140Q)). Primary HD(140Q/140Q) cortical neurons took up significantly less glucose than did WT neurons. Expression of permanently inactive and permanently active forms of Rab11 correspondingly altered glucose uptake in WT neurons, suggesting that normal activity of Rab11 is needed for neuronal uptake of glucose. It is known that Rab11 activity is diminished in HD(140Q/140Q) neurons. Expression of dominant active Rab11 to enhance the activity of Rab11 normalized glucose uptake in HD(140Q/140Q) neurons. These results suggest that deficient activity of Rab11 is a novel mechanism for glucose hypometabolism in HD.

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Crossref · 10.1016/j.bbrc.2012.04.070

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Research works printed but not linked: 27

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Metadata

Authors
Li, X., Valencia, A., McClory, H., Sapp, E., Kegel, K. B., & DiFiglia, M.
Venue
Biochemical and Biophysical Research Communications
Publisher
Elsevier BV
Published
2012-05
Volume
421
Issue
4
Pages
727-730
ISSN
0006-291X
DOI
10.1016/j.bbrc.2012.04.070
Cited by
33
References
0
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Funders
  • Hereditary Disease Foundation
  • CHDI Foundation to XL

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