High‐fat diet in a mouse insulin‐resistant model induces widespread rewiring of the phosphotyrosine signaling network
Name
msb.20198849.pdf
Description
Published version
Size
2.89 MB
Format
Adobe PDF
Checksum (MD5)
bbf047324931eb2a197c31fa0e9187ae
Author(s)
Dittmann, Antje
Soltero, Nina L.
Morshed, Nader
Mana, Mana
Yilmaz, Omer H.
White, Forest M.
Date Issued
August 2019
Journal
Molecular Systems Biology
Publisher
EMBO
Citation
Dittmann, Antje et al. "High‐fat diet in a mouse insulin‐resistant model induces widespread rewiring of the phosphotyrosine signaling network." Molecular Systems Biology 15 (2019): e8849 © 2019 The Author(s)
Version
Final published version
Abstract
Obesity-associated type 2 diabetes and accompanying diseases have developed into a leading human health risk across industrialized and developing countries. The complex molecular underpinnings of how lipid overload and lipid metabolites lead to the deregulation of metabolic processes are incompletely understood. We assessed hepatic post-translational alterations in response to treatment of cells with saturated and unsaturated free fatty acids and the consumption of a high-fat diet by mice. These data revealed widespread tyrosine phosphorylation changes affecting a large number of enzymes involved in metabolic processes as well as canonical receptor-mediated signal transduction networks. Targeting two of the most prominently affected molecular features in our data, SRC-family kinase activity and elevated reactive oxygen species, significantly abrogated the effects of saturated fat exposure in vitro and high-fat diet in vivo. In summary, we present a comprehensive view of diet-induced alterations of tyrosine signaling networks, including proteins involved in fundamental metabolic pathways.
Subjects
General Biochemistry, Genetics and Molecular Biology
Computational Theory and Mathematics
General Immunology and Microbiology
Applied Mathematics
General Agricultural and Biological Sciences
Information Systems
MIT Department
Massachusetts Institute of Technology. Department of Biological Engineering
Koch Institute for Integrative Cancer Research at MIT
Terms of Use
Creative Commons Attribution 4.0 International license
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.15252/msb.20198849
