Evidence map›Paper›PMID 25468647›Full record

ArticleMolecular genetics and metabolism2015

Mathematical modeling of the insulin signal transduction pathway for prediction of insulin sensitivity from expression data.

Clark K Ho, Lola Rahib, James C Liao, Ganesh Sriram, Katrina M Dipple

Abstract read
In one paragraph

Article in Molecular genetics and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Review
  2. Article
  3. Insulin Signaling Pathway Model in Adipocyte Cells.Current pharmaceutical design · 2023
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
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

5 authors.

Clark K HoBiomedical Engineering Interdepartmental Program, Henry Samueli School of Engineering and Applied Science at UCLA, USA.
Lola RahibBiomedical Engineering Interdepartmental Program, Henry Samueli School of Engineering and Applied Science at UCLA, USA.
James C LiaoBiomedical Engineering Interdepartmental Program, Henry Samueli School of Engineering and Applied Science at UCLA, USA; Department of Chemical and Biomolecular Engineering, Henry Samueli School of Engineering and Applied Science at UCLA, USA.
Ganesh SriramDepartment of Chemical and Biomolecular Engineering, Henry Samueli School of Engineering and Applied Science at UCLA, USA; Department of Human Genetics, David Geffen School of Medicine at UCLA, USA.
Katrina M DippleBiomedical Engineering Interdepartmental Program, Henry Samueli School of Engineering and Applied Science at UCLA, USA; Department of Human Genetics, David Geffen School of Medicine at UCLA, USA; Department of Pediatrics, David Geffen School of Medicine at UCLA, USA; Mattel Children's Hospital at UCLA, USA. Electronic address: kdipple@ucla.edu.

Funding

Biotechnology Training in Biomedical Sciences and EngineeringT32GM067555 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GU, ZHEN · 2005 to 2019
$2.8M
NIGMS NIH HHS T32 GM067555NIGMS NIH HHS T32GM067555
6 · The paper itself

Abstract

Mathematical models of biological pathways facilitate a systems biology approach to medicine. However, these models need to be updated to reflect the latest available knowledge of the underlying pathways. We developed a mathematical model of the insulin signal transduction pathway by expanding the last major previously reported model and incorporating pathway components elucidated since the original model was reported. Furthermore, we show that inputting gene expression data of key components of the insulin signal transduction pathway leads to sensible predictions of glucose clearance rates in agreement with reported clinical measurements. In one set of simulations, our model predicted that glycerol kinase knockout mice have reduced GLUT4 translocation, and consequently, reduced glucose uptake. Additionally, a comparison of our extended model with the original model showed that the added pathway components improve simulations of glucose clearance rates. We anticipate this expanded model to be a useful tool for predicting insulin sensitivity in mammalian tissues with altered expression protein phosphorylation or mRNA levels of insulin signal transduction pathway components.

Indexed as

Insulin ResistanceModels, BiologicalSignal TransductionAnimalsGene Expression ProfilingGlucoseGlucose Transporter Type 4Glycerol KinaseInsulinMiceMice, KnockoutPhosphorylationGlucoseGlucose Transporter Type 4Glycerol KinaseInsulinInsulin sensitivityInsulin signal transduction pathwayMathematical modeling

Identifiers

PMID25468647
PMCPMC4319670

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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.