Evidence map›Paper›PMID 22859932›Full record

ArticlePloS one2012

The transcriptional coactivators p/CIP and SRC-1 control insulin resistance through IRS1 in obesity models.

Zhiyong Wang, O Jameel Shah, Tony Hunter

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Nuclear Mechanisms of Insulin Resistance.Trends in cell biology · 2016
    Review
  9. Dietary approaches to stop hypertension influence on insulin receptor substrate-1gene expression: A randomized controlled clinical trial.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2015
    Article
  10. Review
  11. Can an oral antidiabetic (rosiglitazone) be of benefit in leukemia treatment?Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2015
    Article
  12. Review
  13. Review
  14. 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

3 authors at 1 institution in 1 country.

Zhiyong WangMolecular and Cell Biology Laboratory, Salk Institute for Biological Studies, La Jolla, California, United States of America. zwang@salk.edu
O Jameel Shah
Tony Hunter
Salk Institute for Biological Studies · US

Funding

Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Ye Zheng · 1985 to 2026
$82.8M
SIGNAL TRANSDUCTION BY TYROSINE PHOSPHORYLATIONR01CA082683 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI HUNTER, TONY R. · 1999 to 2019
$12.2M
NCI NIH HHS CA14195NCI NIH HHS CA82683NCI NIH HHS P30 CA014195NCI NIH HHS R01 CA082683
6 · The paper itself

Abstract

Three p160 family members, p/CIP, SRC1, and TIF2, have been identified as transcriptional coactivators for nuclear hormone receptors and other transcription factors in vitro. In a previous study, we reported initial characterization of the obesity-resistant phenotypes of p/CIP and SRC-1 double knockout (DKO) mice, which exhibit increased energy expenditure, and suggested that nuclear hormone receptor target genes were involved in these phenotypes. In this study, we demonstrate that p/CIP and SRC1 control insulin signaling in a cell-autonomous manner both in vitro and in vivo. Genetic deletion of p/CIP and SRC-1 increases glucose uptake and enhances insulin sensitivity in both regular chow- and high fat diet-fed DKO mice despite increased food intake. Interestingly, we discover that loss of p/CIP and SRC-1 results in resistance to age-related obesity and glucose intolerance. We show that expression levels of a key insulin signaling component, insulin receptor substrate 1 (IRS1), are significantly increased in two cell lines representing fat and muscle lineages with p/CIP and SRC-1 deletions and in white adipose tissue and skeletal muscle of DKO mice; this may account for increased glucose metabolism and insulin sensitivity. This is the first evidence that the p160 coactivators control insulin signaling and glucose metabolism through IRS1. Therefore, our studies indicate that p/CIP and SRC-1 are potential therapeutic targets not only for obesity but also for diabetes.

Indexed as

Insulin ResistanceAdiponectinAdipose Tissue, WhiteAnimalsBlood GlucoseDiet, High-FatDisease Models, AnimalGene ExpressionGene Knockdown TechniquesGlucose Tolerance TestInsulin Receptor Substrate ProteinsMaleMiceMice, KnockoutMuscle, SkeletalNIH 3T3 CellsAdiponectinBlood GlucoseInsulin Receptor Substrate ProteinsIrs1 protein, mouseNcoa1 protein, mouseNcoa3 protein, mouseNuclear Receptor Coactivator 1Nuclear Receptor Coactivator 3RNA, Small Interfering

Identifiers

PMID22859932
PMCPMC3409189
OpenAlexW1990225338

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.