ArticleMetabolism: clinical and experimental2015
Hepatic proteomic analysis revealed altered metabolic pathways in insulin resistant Akt1(+/-)/Akt2(-/-) mice.
Article in Metabolism: clinical and experimental, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Functional characterization of CD49fJournal of molecular histology · 2022Article
- Multi-omics profiling: the way towards precision medicine in metabolic diseases.Journal of molecular cell biology · 2021Article
- Protein Expression Profile of Twenty-Week-Old Diabetic db/db and Non-Diabetic Mice Livers: A Proteomic and Bioinformatic Analysis.Biomolecules · 2018Article
- Improvement in glycemia after glucose or insulin overload in leptin-infused rats is associated with insulin-related activation of hepatic glucose metabolism.Nutrition & metabolism · 2016Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveThe aim of this study was to identify liver proteome changes in a mouse model of severe insulin resistance and markedly decreased leptin levels.
methodsTwo-dimensional differential gel electrophoresis was utilized to identify liver proteome changes in AKT1(+/-)/AKT2(-/-) mice. Proteins with altered levels were identified with tandem mass spectrometry. Ingenuity Pathway Analysis was performed for the interpretation of the biological significance of the observed proteomic changes.
results11 proteins were identified from 2 biological replicates to be differentially expressed by a ratio of at least 1.3 between age-matched insulin resistant (Akt1(+/-)/Akt2(-/-)) and wild type mice. Albumin and mitochondrial ornithine aminotransferase were detected from multiple spots, which suggest post-translational modifications. Enzymes of the urea cycle were common members of top regulated pathways.
conclusionOur results help to unveil the regulation of the liver proteome underlying altered metabolism in an animal model of severe insulin resistance.
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