Evidence map›Paper›PMID 19841271›Full record

Trial reportProceedings of the National Academy of Sciences of the United States of America2009

Mechanisms of human insulin resistance and thiazolidinedione-mediated insulin sensitization.

D D Sears, G Hsiao, A Hsiao, J G Yu, C H Courtney, J M Ofrecio, J Chapman, S Subramaniam

Open access · greenAbstract readClinical Trial
In one paragraph

Trial report in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

105 citing papers in PubMed, 1 synthesis or guideline pooled it, 176 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  7. Article
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  14. The role of BCAA metabolism in metabolic health and disease.Experimental & molecular medicine · 2024
    Review
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45 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

D D SearsDepartment of Medicine, University of California at San Diego, La Jolla, CA 92093, USA. dsears@ucsd.edu
G Hsiao
A Hsiao
J G Yu
C H Courtney
J M Ofrecio
J Chapman
S Subramaniam
University of California, San Diego · USLa Jolla Bioengineering Institute · USPfizer (United States) · US

Funding

STEROL LIPIDSU54GM069338 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DENNIS, EDWARD A · 2003 to 2013
$72.2M
The Interaction of Neuroendocrine Repro. Function and Metabolic SignalingU54HD012303 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MELLON, PAMELA L · 1999 to 2013
$18.0M
Transcriptional Genomics CoreP01DK074868 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASS, CHRISTOPHER K · 2007 to 2016
$16.6M
INSULIN RECEPTORS AND THE GLUCOSE TRANSPORT SYSTEMR01DK033651 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI OLEFSKY, JERROLD MICHAEL · 1986 to 2013
$2.2M
Reconstruction and Modeling of Networks Involved in Cardiomyoctye DifferentiationR33HL087375 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SUBRAMANIAM, SHANKAR · 2007 to 2009
$1.1M
IDENTIFICATION AND STUDY OF PPARgamma-REGULATED GENESK01DK062025 · NIDDK · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI SEARS, DOROTHY D · 2002 to 2004
$335k
NHLBI NIH HHS R33 HL087375NHLBI NIH HHS R33-HL087375NICHD NIH HHS U54 HD012303NICHD NIH HHS U54-HD012303NIDDK NIH HHS K01 DK062025NIDDK NIH HHS K01-DK62025NIDDK NIH HHS P01 DK074868NIDDK NIH HHS P01-DK074868NIDDK NIH HHS R01 DK033651NIDDK NIH HHS R01-DK033651NIGMS NIH HHS U54 GM069338NIGMS NIH HHS U54-GM69338
6 · The paper itself

Abstract

Cellular and tissue defects associated with insulin resistance are coincident with transcriptional abnormalities and are improved after insulin sensitization with thiazolidinedione (TZD) PPARgamma ligands. We characterized 72 human subjects by relating their clinical phenotypes with functional pathway alterations. We transcriptionally profiled 364 biopsies harvested before and after hyperinsulinemic-euglycemic clamp studies, at baseline and after 3-month TZD treatment. We have identified molecular and functional characteristics of insulin resistant subjects and distinctions between TZD treatment responder and nonresponder subjects. Insulin resistant subjects exhibited alterations in skeletal muscle (e.g., glycolytic flux and intramuscular adipocytes) and adipose tissue (e.g., mitochondrial metabolism and inflammation) that improved relative to TZD-induced insulin sensitization. Pre-TZD treatment expression of MLXIP in muscle and HLA-DRB1 in adipose tissue from insulin resistant subjects was linearly predictive of post-TZD insulin sensitization. We have uniquely characterized coordinated cellular and tissue functional pathways that are characteristic of insulin resistance, TZD-induced insulin sensitization, and potential TZD responsiveness.

Indexed as

Insulin ResistanceAdipocytesAdipose TissueBiomarkersGene Expression ProfilingGene Expression RegulationGlucoseHumansInflammationInsulinMitochondriaMuscle, SkeletalThiazolidinedionesBiomarkersGlucoseInsulinThiazolidinediones

Identifiers

PMID19841271
PMCPMC2763882
OpenAlexW2021805976

What OpenQuestion holds

Textmetadata
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.