Show simple item record

AuthorPepin, Mark E.dc.contributor.author
AuthorKoentges, Christophdc.contributor.author
AuthorPfeil, Katharinadc.contributor.author
AuthorGollmer, Johannesdc.contributor.author
AuthorKersting, Sophia Katharinadc.contributor.author
AuthorWiese, Sebastian Edgardc.contributor.author
AuthorHoffmann, Michael Marcusdc.contributor.author
AuthorOdening, Katja Elisabethdc.contributor.author
AuthorZur Mühlen, Constantin vondc.contributor.author
AuthorDiehl, Philippdc.contributor.author
AuthorStachon, Peterdc.contributor.author
AuthorWolf, Dennisdc.contributor.author
AuthorWende, Adam R.dc.contributor.author
AuthorBode, Christophdc.contributor.author
AuthorZirlik, Andreasdc.contributor.author
AuthorBugger, Heikodc.contributor.author
Date of accession2020-07-06T08:27:25Zdc.date.accessioned
Available in OPARU since2020-07-06T08:27:25Zdc.date.available
Date of first publication2019-12-13dc.date.issued
AbstractDecreased serum adiponectin levels in type 2 diabetes has been linked to the onset of mitochondrial dysfunction in diabetic complications by impairing AMPK-SIRT1-PGC-1α signaling via impaired adiponectin receptor 1 (AdipoR1) signaling. Here, we aimed to characterize the previously undefined role of disrupted AdipoR1 signaling on the mitochondrial protein composition of cardiac, renal, and hepatic tissues as three organs principally associated with diabetic complications. Comparative proteomics were performed in mitochondria isolated from the heart, kidneys and liver of Adipor1−/− mice. A total of 790, 1,573, and 1,833 proteins were identified in cardiac, renal and hepatic mitochondria, respectively. While 121, 98, and 78 proteins were differentially regulated in cardiac, renal, and hepatic tissue of Adipor1−/− mice, respectively; only 15 proteins were regulated in the same direction across all investigated tissues. Enrichment analysis of differentially expressed proteins revealed disproportionate representation of proteins involved in oxidative phosphorylation conserved across tissue types. Curated pathway analysis identified HNF4, NRF1, LONP, RICTOR, SURF1, insulin receptor, and PGC-1α as candidate upstream regulators. In high fat-fed non-transgenic mice with obesity and insulin resistance, AdipoR1 gene expression was markedly reduced in heart (−70%), kidney (−80%), and liver (−90%) (all P < 0.05) as compared to low fat-fed mice. NRF1 was the only upstream regulator downregulated both in Adipor1−/− mice and in high fat-fed mice, suggesting common mechanisms of regulation. Thus, AdipoR1 signaling regulates mitochondrial protein composition across all investigated tissues in a functionally conserved, yet molecularly distinct, manner. The biological significance and potential implications of impaired AdipoR1 signaling are discussed.dc.description.abstract
Languageendc.language.iso
PublisherUniversität Ulmdc.publisher
LicenseCC BY 4.0 Internationaldc.rights
Link to license texthttps://creativecommons.org/licenses/by/4.0/dc.rights.uri
Dewey Decimal GroupDDC 570 / Life sciencesdc.subject.ddc
Dewey Decimal GroupDDC 610 / Medicine & healthdc.subject.ddc
MeSHMitochondriadc.subject.mesh
MeSHAdiponectindc.subject.mesh
MeSHReceptors, Adiponectindc.subject.mesh
MeSHDiabetes mellitus, Type 2dc.subject.mesh
MeSHHeartdc.subject.mesh
MeSHProteomedc.subject.mesh
TitleDysregulation of the mitochondrial proteome occurs in mice lacking adiponectin receptor 1dc.title
Resource typeWissenschaftlicher Artikeldc.type
SWORD Date2019-12-19T17:48:17Zdc.date.updated
VersionpublishedVersiondc.description.version
DOIhttp://dx.doi.org/10.18725/OPARU-32222dc.identifier.doi
URNhttp://nbn-resolving.de/urn:nbn:de:bsz:289-oparu-32284-6dc.identifier.urn
GNDMitochondriumdc.subject.gnd
GNDDiabetes mellitus Typ 2dc.subject.gnd
GNDHerzdc.subject.gnd
GNDProteomdc.subject.gnd
FacultyMedizinische Fakultätuulm.affiliationGeneral
InstitutionMassenspektrometrie und Proteomicsuulm.affiliationSpecific
Peer reviewjauulm.peerReview
DCMI TypeCollectionuulm.typeDCMI
CategoryPublikationenuulm.category
In cooperation withAlbert-Ludwigs-Universität Freiburguulm.cooperation
In cooperation withThe University of Alabama at Birminghamuulm.cooperation
In cooperation withMedizinische Universität Grazuulm.cooperation
Is Supplemented Byhttps://www.frontiersin.org/articles/10.3389/fendo.2019.00872/full#supplementary-materialuulm.relation.isSupplementedBy
DOI of original publication10.3389/fendo.2019.00872dc.relation1.doi
Source - Title of sourceFrontiers in Endocrinologysource.title
Source - Place of publicationFrontiers Mediasource.publisher
Source - Volume10source.volume
Source - Year2019source.year
Source - Article number872source.articleNumber
Source - ISSN1664-2392source.identifier.issn
FundingGerman Heart Research Foundation [F-01-16]uulm.funding
University Bibliographyjauulm.unibibliographie


Files in this item

Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail

This item appears in the following Collection(s)

Show simple item record

CC BY 4.0 International
Except where otherwise noted, this item's license is described as CC BY 4.0 International