dc.contributor.author
Brachs, Sebastian
dc.contributor.author
Winkel, Angelika F.
dc.contributor.author
Polack, James
dc.contributor.author
Tang, Hui
dc.contributor.author
Brachs, Maria
dc.contributor.author
Margerie, Daniel
dc.contributor.author
Brunner, Bodo
dc.contributor.author
Jahn-Hofmann, Kerstin
dc.contributor.author
Ruetten, Hartmut
dc.contributor.author
Spranger, Joachim
dc.contributor.author
Schmoll, Dieter
dc.date.accessioned
2018-06-08T10:59:38Z
dc.date.available
2017-01-09T10:18:55.338Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/21449
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-24742
dc.description.abstract
The transcription factor NF-E2-related factor 2 (Nrf2) induces cytoprotective
genes, but has also been linked to the regulation of hepatic energy
metabolism. In order to assess the pharmacological potential of hepatic Nrf2
activation in metabolic disease, Nrf2 was activated over 7 weeks in mice on
Western diet using two different siRNAs against kelch-like ECH-associated
protein 1 (Keap1), the inhibitory protein of Nrf2. Whole genome expression
analysis followed by pathway analysis demonstrated successful knock-down of
Keap1 expression and induction of Nrf2-dependent genes involved in anti-
oxidative stress defense and biotransformation, proving the activation of Nrf2
by the siRNAs against Keap1. Neither the expression of fatty acid- nor
carbohydrate-handling proteins was regulated by Keap1 knock-down. Metabolic
profiling of the animals did also not show effects on plasma and hepatic
lipids, energy expenditure or glucose tolerance. The data indicate that
hepatic Keap1/Nrf2 is not a major regulator of glucose or lipid metabolism in
mice.
en
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit
dc.title
Chronic Activation of Hepatic Nrf2 Has No Major Effect on Fatty Acid and
Glucose Metabolism in Adult Mice
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation
PLoS ONE. - 11 (2016), 11, Artikel Nr. e0166110
dcterms.bibliographicCitation.doi
10.1371/journal.pone.0166110
dcterms.bibliographicCitation.url
http://dx.doi.org/10.1371/journal.pone.0166110
refubium.affiliation
Charité - Universitätsmedizin Berlin
de
refubium.mycore.fudocsId
FUDOCS_document_000000026100
refubium.note.author
Der Artike wurde in einer reinen Open-Access-Zeitschrift publziert.
refubium.resourceType.isindependentpub
no
refubium.mycore.derivateId
FUDOCS_derivate_000000007488
dcterms.accessRights.openaire
open access