Evidence map›Paper›PMID 31464373›Full record

ArticleMolecular systems biology2019

High-fat diet in a mouse insulin-resistant model induces widespread rewiring of the phosphotyrosine signaling network.

Antje Dittmann, Norman J Kennedy, Nina L Soltero, Nader Morshed, Miyeko D Mana, Ömer H Yilmaz, Roger J Davis, Forest M White

Open access · goldAbstract read
In one paragraph

Article in Molecular systems biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 46 citations in OpenAlex.

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  17. Protective Effect of a Mixture ofEvidence-based complementary and alternative medicine : eCAM · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Antje DittmannThe David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.
Norman J KennedyProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, USA.
Nina L SolteroThe David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.
Nader MorshedThe David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.
Miyeko D ManaThe David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.
Ömer H YilmazThe David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.
Roger J DavisProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, USA.ORCID 0000-0002-0130-1652
Forest M WhiteThe David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID 0000-0002-1545-1651
Massachusetts Institute of Technology · USBroad Institute · USHoward Hughes Medical Institute · USUniversity of Massachusetts Chan Medical School · US

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI Paula T Hammond · 1985 to 2026
$93.9M
Systems Biology of Insulin ResistanceR24DK090963 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DAVIS, ROGER J. · 2011 to 2014
$8.4M
Metabolic Stress SignalingR01DK107220 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DAVIS, ROGER J. · 2016 to 2023
$3.6M
Dietary control of stem cells in physiology and cancerR01CA211184 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI YILMAZ, OMER · 2017 to 2021
$2.0M
NCI NIH HHS P30 CA014051NCI NIH HHS R01 CA211184NIDDK NIH HHS R01 DK107220NIDDK NIH HHS R24 DK090963
6 · The paper itself

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.

Indexed as

Protein Processing, Post-TranslationalAnimalsCell Line, TumorDiabetes Mellitus, Type 2Diet, High-FatDisease Models, AnimalFatty AcidsHepatocytesLiverMaleMiceMice, Inbred C57BLMice, TransgenicObesityPhosphorylationPhosphotyrosineFatty AcidsPhosphotyrosineProtein Kinase InhibitorsReactive Oxygen Speciessrc-Family Kinasesdiabetesfree fatty acidshigh-fat dietobesityphosphoproteomics

Identifiers

PMID31464373
PMCPMC6674232
OpenAlexW2964645477

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.