Evidence map›Paper›PMID 23351585›Full record

ReviewJournal of clinical lipidology

Genetic determinants of cardiometabolic risk: a proposed model for phenotype association and interaction.

Piers R Blackett, Dharambir K Sanghera

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of clinical lipidology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
–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

21 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Parental non-alcoholic fatty liver disease increases risk of non-alcoholic fatty liver disease in offspring.Liver international : official journal of the International Association for the Study of the Liver · 2019
    Article
  13. Article
  14. Review
  15. Article
  16. The Flexibility of Ectopic Lipids.International journal of molecular sciences · 2016
    Review
  17. Article
  18. Article
  19. Article
  20. Nonalcoholic fatty liver disease and cardiovascular disease.World journal of gastroenterology · 2014
    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

2 authors.

Piers R BlackettDepartment of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
Dharambir K Sanghera

Funding

Genome-wide Association Scan to Identify Risk Genes for Type 2 Diabetes in AsianR01DK082766 · NIDDK · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI SANGHERA, DHARAMBIR K. · 2009 to 2011
$2.3M
Indo-US Collaboration in Genomic Studies on DiabetesK01TW006087 · FIC · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SANGHERA, DHARAMBIR K · 2002 to 2007
$778k
FIC NIH HHS K01 TW006087FIC NIH HHS K01TW006087NIDDK NIH HHS R01 DK082766NIDDK NIH HHS R01DK082766
6 · The paper itself

Abstract

This review provides a translational and unifying summary of metabolic syndrome genetics and highlights evidence that genetic studies are starting to unravel and untangle origins of the complex and challenging cluster of disease phenotypes. The associated genes effectively express in the brain, liver, kidney, arterial endothelium, adipocytes, myocytes, and β cells. Progression of syndrome traits has been associated with ectopic lipid accumulation in the arterial wall, visceral adipocytes, myocytes, and liver. Thus, it follows that the genetics of dyslipidemia, obesity, and nonalcoholic fatty liver disease are central in triggering progression of the syndrome to overt expression of disease traits and have become a key focus of interest for early detection and for designing prevention and treatments. To support the "birds' eye view" approach, we provide a road-map depicting commonality and interrelationships between the traits and their genetic and environmental determinants based on known risk factors, metabolic pathways, pharmacologic targets, treatment responses, gene networks, pleiotropy, and association with circadian rhythm. Although only a small portion of the known heritability is accounted for and there is insufficient support for clinical application of gene-based prediction models, there is direction and encouraging progress in a rapidly moving field that is beginning to show clinical relevance.

Indexed as

Models, BiologicalAlpha-Ketoglutarate-Dependent Dioxygenase FTOCholesterol Ester Transfer ProteinsDyslipidemiasFatty LiverGenome-Wide Association StudyHumansHypertensionHypothalamic DiseasesInsulin-Secreting CellsLipoproteinsMetabolic Networks and PathwaysNon-alcoholic Fatty Liver DiseasePhenotypeProteinsAlpha-Ketoglutarate-Dependent Dioxygenase FTOCETP protein, humanCholesterol Ester Transfer ProteinsFTO protein, humanLipoproteinsProteins

Identifiers

PMID23351585
PMCPMC3559023

What OpenQuestion holds

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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.