Progressive Impairment of Lactate-based Gluconeogenesis in the Huntington's Disease Mouse Model R6/2

Research output: Contribution to journalConference abstract in journalResearchpeer-review

Standard

Progressive Impairment of Lactate-based Gluconeogenesis in the Huntington's Disease Mouse Model R6/2. / Nielsen, Signe Marie Borch; Hasholt, Lis; Nørremølle, Anne; Josefsen, Knud Elnegaard.

In: PLoS Currents, Vol. 7, 20.04.2015.

Research output: Contribution to journalConference abstract in journalResearchpeer-review

Harvard

Nielsen, SMB, Hasholt, L, Nørremølle, A & Josefsen, KE 2015, 'Progressive Impairment of Lactate-based Gluconeogenesis in the Huntington's Disease Mouse Model R6/2', PLoS Currents, vol. 7. https://doi.org/10.1371/currents.hd.019b33aae1c519e6e8b68e7cf3e7818e

APA

Nielsen, S. M. B., Hasholt, L., Nørremølle, A., & Josefsen, K. E. (2015). Progressive Impairment of Lactate-based Gluconeogenesis in the Huntington's Disease Mouse Model R6/2. PLoS Currents, 7. https://doi.org/10.1371/currents.hd.019b33aae1c519e6e8b68e7cf3e7818e

Vancouver

Nielsen SMB, Hasholt L, Nørremølle A, Josefsen KE. Progressive Impairment of Lactate-based Gluconeogenesis in the Huntington's Disease Mouse Model R6/2. PLoS Currents. 2015 Apr 20;7. https://doi.org/10.1371/currents.hd.019b33aae1c519e6e8b68e7cf3e7818e

Author

Nielsen, Signe Marie Borch ; Hasholt, Lis ; Nørremølle, Anne ; Josefsen, Knud Elnegaard. / Progressive Impairment of Lactate-based Gluconeogenesis in the Huntington's Disease Mouse Model R6/2. In: PLoS Currents. 2015 ; Vol. 7.

Bibtex

@article{ac01546791d14cde8c4e05078a78eca1,
title = "Progressive Impairment of Lactate-based Gluconeogenesis in the Huntington's Disease Mouse Model R6/2",
abstract = "Huntington's disease (HD) is a neurodegenerative illness, where selective neuronal loss in the brain caused by expression of mutant huntingtin protein leads to motor dysfunction and cognitive decline in addition to peripheral metabolic changes. In this study we confirm our previous observation of impairment of lactate-based hepatic gluconeogenesis in the transgenic HD mouse model R6/2 and determine that the defect manifests very early and progresses in severity with disease development, indicating a potential to explore this defect in a biomarker context. Moreover, R6/2 animals displayed lower blood glucose levels during prolonged fasting compared to wild type animals.",
author = "Nielsen, {Signe Marie Borch} and Lis Hasholt and Anne N{\o}rrem{\o}lle and Josefsen, {Knud Elnegaard}",
year = "2015",
month = apr,
day = "20",
doi = "10.1371/currents.hd.019b33aae1c519e6e8b68e7cf3e7818e",
language = "English",
volume = "7",
journal = "P L o S Currents",
issn = "2157-3999",
publisher = "Public Library of Science",

}

RIS

TY - ABST

T1 - Progressive Impairment of Lactate-based Gluconeogenesis in the Huntington's Disease Mouse Model R6/2

AU - Nielsen, Signe Marie Borch

AU - Hasholt, Lis

AU - Nørremølle, Anne

AU - Josefsen, Knud Elnegaard

PY - 2015/4/20

Y1 - 2015/4/20

N2 - Huntington's disease (HD) is a neurodegenerative illness, where selective neuronal loss in the brain caused by expression of mutant huntingtin protein leads to motor dysfunction and cognitive decline in addition to peripheral metabolic changes. In this study we confirm our previous observation of impairment of lactate-based hepatic gluconeogenesis in the transgenic HD mouse model R6/2 and determine that the defect manifests very early and progresses in severity with disease development, indicating a potential to explore this defect in a biomarker context. Moreover, R6/2 animals displayed lower blood glucose levels during prolonged fasting compared to wild type animals.

AB - Huntington's disease (HD) is a neurodegenerative illness, where selective neuronal loss in the brain caused by expression of mutant huntingtin protein leads to motor dysfunction and cognitive decline in addition to peripheral metabolic changes. In this study we confirm our previous observation of impairment of lactate-based hepatic gluconeogenesis in the transgenic HD mouse model R6/2 and determine that the defect manifests very early and progresses in severity with disease development, indicating a potential to explore this defect in a biomarker context. Moreover, R6/2 animals displayed lower blood glucose levels during prolonged fasting compared to wild type animals.

U2 - 10.1371/currents.hd.019b33aae1c519e6e8b68e7cf3e7818e

DO - 10.1371/currents.hd.019b33aae1c519e6e8b68e7cf3e7818e

M3 - Conference abstract in journal

C2 - 26064782

VL - 7

JO - P L o S Currents

JF - P L o S Currents

SN - 2157-3999

ER -

ID: 161031532