Evidence map›Paper›PMID 24531647›Full record

ArticleInternational journal of obesity (2005)2014

NAG-1/GDF-15 prevents obesity by increasing thermogenesis, lipolysis and oxidative metabolism.

K Chrysovergis, X Wang, J Kosak, S-H Lee, J S Kim, J F Foley, G Travlos, S Singh, S J Baek, T E Eling

Open access · greenAbstract read
In one paragraph

Article in International journal of obesity (2005), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed, 1 pooled it
6.9field-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

132 citing papers in PubMed, 1 synthesis or guideline pooled it, 235 citations in OpenAlex.

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  7. GDF-15 Levels in Cirrhosis Are Linked to Hepatic Fibrogenesis, Bacterial Translocation, and Worse Clinical Outcomes.Liver international : official journal of the International Association for the Study of the Liver · 2026
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72 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

10 authors at 4 institutions in 1 country.

K ChrysovergisLaboratory of Molecular Carcinogenesis, NIEHS, NIH, Research Triangle Park, NC, USA.
X WangLaboratory of Molecular Carcinogenesis, NIEHS, NIH, Research Triangle Park, NC, USA.
J KosakLaboratory of Molecular Carcinogenesis, NIEHS, NIH, Research Triangle Park, NC, USA.
S-H LeeDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN, USA.
J S Kim1] Laboratory of Molecular Carcinogenesis, NIEHS, NIH, Research Triangle Park, NC, USA [2] Department of Biological Sciences, Andong National University, Andong, South Korea.
J F FoleyCellular and Molecular Pathology Branch, NIEHS, NIH, Research Triangle Park, NC, USA.
G TravlosCellular and Molecular Pathology Branch, NIEHS, NIH, Research Triangle Park, NC, USA.
S SinghLaboratory of Molecular Carcinogenesis, NIEHS, NIH, Research Triangle Park, NC, USA.
S J BaekDepartment of Biomedical and Diagnostic Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, TN, USA.
T E ElingLaboratory of Molecular Carcinogenesis, NIEHS, NIH, Research Triangle Park, NC, USA.
Research Triangle Park Foundation · USNational Institute of Environmental Health Sciences · USUniversity of Tennessee at Knoxville · USTriangle · US

Funding

Anti-carcinogenic Activity Of Cox inhibitors and NAG-1ZIAES010016 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI ELING, THOMAS · 2009 to 2013
$8.3M
Mediation of Anti-carcinogenic Activity Of NSAIDSZ01ES010016 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI ELING, THOMAS · 1999 to 2008
$2.8M
Intramural NIH HHS Z01 ES010016Intramural NIH HHS ZIA ES010016
6 · The paper itself

Abstract

objectiveObesity is a major health problem associated with high morbidity and mortality. NSAID-activated gene (NAG-1) is a TGF-β superfamily member reported to alter adipose tissue levels in mice. We investigated whether hNAG-1 acts as a regulator of adiposity and energy metabolism. DESIGN/SUBJECTS: hNAG-1 mice, ubiquitously expressing hNAG-1, were placed on a control or high-fat diet for 12 weeks. hNAG-1-expressing B16/F10 melanoma cells were used in a xenograft model to deliver hNAG-1 to obese C57BL/6 mice.

resultsAs compared with wild-type littermates, transgenic hNAG-1 mice have less white fat and brown fat despite equivalent food intake, improved glucose tolerance, lower insulin levels and are resistant to dietary- and genetic-induced obesity. hNAG-1 mice are more metabolically active with higher energy expenditure. Obese C57BL/6 mice treated with hNAG-1-expressing xenografts show decreases in adipose tissue and serum insulin levels. hNAG-1 mice and obese mice treated with hNAG-1-expressing xenografts show increased thermogenic gene expression (UCP1, PGC1α, ECH1, Cox8b, Dio2, Cyc1, PGC1β, PPARα, Elvol3) in brown adipose tissue (BAT) and increased expression of lipolytic genes (Adrb3, ATGL, HSL) in both white adipose tissue (WAT) and BAT, consistent with higher energy metabolism.

conclusionhNAG-1 modulates metabolic activity by increasing the expression of key thermogenic and lipolytic genes in BAT and WAT. hNAG-1 appears to be a novel therapeutic target in preventing and treating obesity and insulin resistance.

Indexed as

LipolysisThermogenesisAdipose TissueAnimalsBlotting, WesternDiet, High-FatEatingEnergy MetabolismEnzyme-Linked Immunosorbent AssayGrowth Differentiation Factor 15HumansInsulin ResistanceMiceMice, Inbred C57BLMice, ObeseObesityGDF15 protein, humanGrowth Differentiation Factor 15

Identifiers

PMID24531647
PMCPMC4135041
OpenAlexW1963540704

What OpenQuestion holds

Textmetadata
LicenceTDM
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.