Evidence map›Paper›PMID 28496128›Full record

ArticleScientific reports2017

A Systems Genetics Approach Identified GPD1L and its Molecular Mechanism for Obesity in Human Adipose Tissue.

Hao He, Dianjianyi Sun, Yong Zeng, Ruifeng Wang, Wei Zhu, Shaolong Cao, George A Bray, Wei Chen, Hui Shen, Frank M Sacks and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 21 citations in OpenAlex.

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  12. Phenolic Compounds Reduce the Fat Content inPharmaceuticals (Basel, Switzerland) · 2020
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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

12 authors at 3 institutions in 1 country.

Hao HeCenter for Bioinformatics and Genomics, Department of Biostatistics and Bioinformatics, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, 70112, USA.
Dianjianyi SunTulane University Obesity Research Center, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, 70112, USA.
Yong ZengCenter for Bioinformatics and Genomics, Department of Biostatistics and Bioinformatics, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, 70112, USA.
Ruifeng WangCenter for Bioinformatics and Genomics, Department of Biostatistics and Bioinformatics, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, 70112, USA.
Wei ZhuCenter for Bioinformatics and Genomics, Department of Biostatistics and Bioinformatics, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, 70112, USA.
Shaolong CaoDepartment of Biomedical Engineering, Tulane University, New Orleans, LA, 70118, USA.
George A BrayPennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA, 70808, USA.
Wei ChenDepartment of Epidemiology, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, 70112, USA.
Hui ShenCenter for Bioinformatics and Genomics, Department of Biostatistics and Bioinformatics, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, 70112, USA.
Frank M SacksDepartment of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, 02115, USA.
Lu QiTulane University Obesity Research Center, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, 70112, USA.
Hong-Wen DengCenter for Bioinformatics and Genomics, Department of Biostatistics and Bioinformatics, Tulane University School of Public Health and Tropical Medicine, New Orleans, LA, 70112, USA. hdeng2@tulane.edu.
Tulane University · USLouisiana State University · USHarvard University · US

Funding

Tulane COBRE in Cardiometabolic Diseases Clinical Research CoreP20GM109036 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI JING CHEN · 2016 to 2026
$25.3M
Transgenic CoreP30DK046200 · NIDDK · TUFTS MEDICAL CENTER · PI GREENBERG, ANDREW S, PERISSI, VALENTINA · 1992 to 2021
$25.0M
Proteome-wide Expression Study of Osteogenic CellsP50AR055081 · NIAMS · UNIVERSITY OF MISSOURI KANSAS CITY · PI DENG, HONG-WEN · 2007 to 2012
$5.0M
Genetic Markers of CHD in Type 2 DiabetesR01HL071981 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI QI, LU · 2003 to 2012
$4.9M
Obesity Genes, Energy Regulation in Response to Weight-Loss DietsR01DK091718 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI QI, LU · 2012 to 2021
$4.5M
Weight-Loss Diet Intervention on Cardiometabolic Factors of Gut MicrobiotaR01DK100383 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI QI, LU · 2014 to 2024
$4.2M
ROBUST AND POWERFUL TEST OF CANDIDATE GENES TO BONE MASSR01AR050496 · NIAMS · UNIVERSITY OF MISSOURI KANSAS CITY · PI DENG, HONG-WEN · 2004 to 2013
$3.8M
Epigenomewide DNA Methylation Study for Osteoporosis RiskR01AR059781 · NIAMS · TULANE UNIVERSITY OF LOUISIANA · PI DENG, HONG-WEN · 2012 to 2016
$3.1M
Identification of Proteins Important for Male OsteoporosisR01AR057049 · NIAMS · UNIVERSITY OF MISSOURI KANSAS CITY · PI DENG, HONG-WEN · 2009 to 2013
$2.4M
Genomic search for bone mass QTLsR01AG026564 · NIA · UNIVERSITY OF MISSOURI KANSAS CITY · PI DENG, HONG-WEN · 2007 to 2010
$2.3M
Genome-wide interactions with diet patterns on long-term weight changeR21HL126024 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI QI, LU · 2015 to 2016
$421k
NHLBI NIH HHS R01 HL071981NHLBI NIH HHS R21 HL126024NIAMS NIH HHS P50 AR055081NIAMS NIH HHS R01 AR050496NIAMS NIH HHS R01 AR057049NIAMS NIH HHS R01 AR059781NIA NIH HHS R01 AG026564NIDDK NIH HHS P30 DK046200NIDDK NIH HHS R01 DK091718NIDDK NIH HHS R01 DK100383NIGMS NIH HHS P20 GM109036
6 · The paper itself

Abstract

To explore novel molecular mechanisms underlying obesity, we applied a systems genetics framework to integrate risk genetic loci from the largest body mass index (BMI) genome-wide association studies (GWAS) meta-analysis with mRNA and microRNA profiling in adipose tissue from 200 subjects. One module was identified to be most significantly associated with obesity and other metabolic traits. We identified eight hub genes which likely play important roles in obesity metabolism and identified microRNAs that significantly negatively correlated with hub genes. This module was preserved in other three test gene expression datasets, and all hub genes were consistently downregulated in obese subjects through the meta-analysis. Gene GPD1L had the highest connectivity and was identified a key causal regulator in the module. Gene GPD1L was significantly negatively correlated with the expression of miR-210, which was experimentally validated that miR-210 regulated GPD1L protein level through direct interaction with its mRNA three prime untranslated region (3'-UTR). GPD1L was found to be upregulated during weight loss and weight maintenance induced by low calorie diet (LCD), while downregulated during weight gain induced by high-fat diet (HFD). The results indicated that increased GPD1L in adipose tissue may have a significant therapeutic potential in reducing obesity and insulin resistance.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseAdipose TissueDatabases, GeneticGene Expression ProfilingGene Expression RegulationGene Regulatory NetworksGlycerolphosphate DehydrogenaseHumansMicroRNAsModels, MolecularObesityReproducibility of ResultsRNA, MessengerGlycerolphosphate DehydrogenaseGPD1L protein, humanMicroRNAsRNA, Messenger

Identifiers

PMID28496128
PMCPMC5431993
OpenAlexW2610926483

What OpenQuestion holds

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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.