Evidence map›Paper›PMID 16249460›Full record

Trial reportDiabetes2005

Sequence variation in PPARG may underlie differential response to troglitazone.

Johanna K Wolford, Kimberly A Yeatts, Sharanjeet K Dhanjal, Mary Helen Black, Anny H Xiang, Thomas A Buchanan, Richard M Watanabe

Open access · bronzeAbstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Diabetes, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 65 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. DisGeNET: a discovery platform for the dynamical exploration of human diseases and their genes.Database : the journal of biological databases and curation · 2015
    Article
  6. Review
  7. Divergent compensatory responses to high-fat diet between C57BL6/J and C57BLKS/J inbred mouse strains.American journal of physiology. Endocrinology and metabolism · 2013
    Article
  8. Review
  9. Type 2 Diabetes Genetics: Beyond GWAS.Journal of diabetes & metabolism · 2012
    Article
  10. Article
  11. Polymorphisms of the peroxisome proliferator-activated receptor γ (PPARγ) gene are associated with osteoporosis.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2011
    Article
  12. Article
  13. Review
  14. The genetics of type 2 diabetes: what have we learned from GWAS?Annals of the New York Academy of Sciences · 2010
    Review
  15. Pharmacogenetics of Anti-Diabetes Drugs.Pharmaceuticals (Basel, Switzerland) · 2010
    Article
  16. Review
  17. Article
  18. Genetic susceptibility to type 2 diabetes and implications for therapy.Journal of diabetes science and technology · 2009
    Review
  19. Article
  20. Clinical translation of genetic predictors for type 2 diabetes.Current opinion in endocrinology, diabetes, and obesity · 2009
    Review
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

7 authors at 2 institutions in 1 country.

Johanna K WolfordGenetic Basis of Human Disease Division, Translational Genomics Research Institute, Phoenix, Arizona, USA.
Kimberly A Yeatts
Sharanjeet K Dhanjal
Mary Helen Black
Anny H Xiang
Thomas A Buchanan
Richard M Watanabe
University of Southern California · USTranslational Genomics Research Institute · US

Funding

ZOPOLRESTAT IN NORMOTENSIVE, TYPE 1 DIA WITH INCIPIENT NEPHROPATHYM01RR000043 · NCRR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ZAIA, JOHN A · 1985 to 2010
$76.4M
NCRR NIH HHS M01 RR000043NCRR NIH HHS M01-RR-00043
6 · The paper itself

Abstract

Thiazolidinediones (TZDs) are peroxisome proliferator-activated receptor-gamma (PPARG) agonists used to treat type 2 diabetes. TZDs can also be used to reduce rates of type 2 diabetes in at-risk individuals. However, a large fraction of TZD-treated patients (30-40%) do not respond to TZD treatment with an improvement in insulin sensitivity (Si). We hypothesized that variation within the gene encoding PPARG may underlie this differential response to TZD therapy. We screened approximately 40 kb of PPARG in 93 nondiabetic Hispanic women (63 responders and 30 nonresponders) with previous gestational diabetes who had participated in the Troglitazone In the Prevention Of Diabetes study. TZD nonresponse was defined as the lower tertile in change in Si after 3 months of treatment. Baseline demographic and clinical measures were not different between responders and nonresponders. We identified and genotyped 131 variants including 126 single nucleotide polymorphisms and 5 insertion-deletion polymorphisms. Linkage disequilibrium analysis identified five haplotype blocks. Eight variants were associated with TZD response (P < 0.05). Three variants were also associated with changes in Si as a continuous variable. Our results suggest that PPARG variation may underlie response to TZD therapy in women at risk for type 2 diabetes.

Indexed as

AdultChromansDiabetes Mellitus, Type 2FemaleHaplotypesHumansHypoglycemic AgentsLinkage DisequilibriumMiddle AgedPharmacogeneticsPhenotypePolymorphism, Single NucleotidePPAR gammaThiazolidinedionesTime FactorsTroglitazoneChromansHypoglycemic AgentsPPAR gammaThiazolidinedionesTroglitazone

Identifiers

PMID16249460
PMCPMC2923445
OpenAlexW2127954231

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.