umu.sePublications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Metabolic Profiling of Multiorgan Samples: Evaluation of MODY5/RCAD Mutant Mice
Umeå University, Faculty of Science and Technology, Department of Chemistry. Accelerator Lab (ACL), Karlsruhe Institute of Technology, Karlsruhe 76344, Germany.ORCID iD: 0000-0002-6294-7844
Show others and affiliations
2018 (English)In: Journal of Proteome Research, ISSN 1535-3893, E-ISSN 1535-3907, Vol. 17, no 7, p. 2293-2306Article in journal (Refereed) Published
Abstract [en]

In the present study, we performed a metabolomics analysis to evaluate a MODY5/RCAD mouse mutant line as a potential model for HNF1B-associated diseases. Gas chromatography time-of-flight mass spectrometry (GC-TOF-MS) of gut, kidney, liver, muscle, pancreas, and plasma samples uncovered the tissue specific metabolite distribution. Orthogonal projections to latent structures discriminant analysis (OPLS-DA) was used to identify the differences between MODY5/RCAD and wild-type mice in each of the tissues. The differences included, for example, increased levels of amino acids in the kidneys and reduced levels of fatty acids in the muscles of the MODY5/RCAD mice. Interestingly, campesterol was found in higher concentrations in the MODY5/RCAD mice, with a four-fold and three-fold increase in kidneys and pancreas, respectively. As expected, the MODY5/RCAD mice displayed signs of impaired renal function in addition to disturbed liver lipid metabolism, with increased lipid and fatty acid accumulation in the liver. From a metabolomics perspective, the MODY5/RCAD model was proven to display a metabolic pattern similar to what would be suspected in HNF1B-associated diseases. These findings were in line with the presumed outcome of the mutation based on the different anatomy and function of the tissues as well as the effect of the mutation on development.

Place, publisher, year, edition, pages
American Chemical Society (ACS), 2018. Vol. 17, no 7, p. 2293-2306
Keywords [en]
HNF1B-associated diseases, metabolomics, OPLS-DA, multiorgan samples, MODY5, RCAD, mouse model
National Category
Endocrinology and Diabetes
Identifiers
URN: urn:nbn:se:umu:diva-150378DOI: 10.1021/acs.jproteome.7b00821ISI: 000438469900004PubMedID: 29873499Scopus ID: 2-s2.0-85048373012OAI: oai:DiVA.org:umu-150378DiVA, id: diva2:1237307
Available from: 2018-08-08 Created: 2018-08-08 Last updated: 2018-08-08Bibliographically approved

Open Access in DiVA

No full text in DiVA

Other links

Publisher's full textPubMedScopus

Authority records BETA

Torell, FridaTrygg, Johan

Search in DiVA

By author/editor
Torell, FridaHaumaitre, CécileTrygg, Johan
By organisation
Department of Chemistry
In the same journal
Journal of Proteome Research
Endocrinology and Diabetes

Search outside of DiVA

GoogleGoogle Scholar

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 130 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf