Evidence map›Paper›PMID 20551328›Full record

ArticleThe Journal of biological chemistry2010

Peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) stimulates VLDL assembly through activation of cell death-inducing DFFA-like effector B (CideB).

Zhouji Chen, Jin Y Norris, Brian N Finck

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 40 citations in OpenAlex.

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  17. Ethanol administration exacerbates the abnormalities in hepatic lipid oxidation in genetically obese mice.American journal of physiology. Gastrointestinal and liver physiology · 2013
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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

3 authors at 1 institution in 1 country.

Zhouji ChenDivision of Geriatrics and Nutritional Science, Department of Medicine, Washington University School of Medicine, St Louis, Missouri 63110, USA. zchen23@wustl.edu
Jin Y Norris
Brian N Finck
Washington University in St. Louis · US

Funding

Washington University DDRCC Supplemental Equipment RequestP30DK052574 · NIDDK · WASHINGTON UNIVERSITY · PI Nicholas O. Davidson · 2000 to 2026
$30.8M
Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Brian N Finck · 1999 to 2026
$30.2M
LIPIN 1 IN THE REGULATION OF HEPATIC LIPID METABOLISMR01DK078187 · NIDDK · WASHINGTON UNIVERSITY · PI FINCK, BRIAN N · 2008 to 2016
$2.8M
ApoB-Proteoglycan Interaction and AtherosclerosisR01HL073939 · NHLBI · WASHINGTON UNIVERSITY · PI CHEN, ZHOUJI · 2003 to 2006
$1.2M
NHLBI NIH HHS R01 HL073939NHLBI NIH HHS R01 HL73939NIDDK NIH HHS P30 DK052574NIDDK NIH HHS P30 DK056341NIDDK NIH HHS P30DK52574NIDDK NIH HHS P30 DK56341NIDDK NIH HHS R01 DK078187
6 · The paper itself

Abstract

Abnormalities in very low density lipoprotein (VLDL) assembly and secretion impact intrahepatic lipid homeostasis, plasma lipoprotein profile, and energy metabolism of distal peripheral tissues. We have evaluated the role of the transcriptional coactivator, the peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha), in VLDL assembly and secretion. PGC-1alpha overexpression in HepG2 cells led to diminished rates of triglyceride (TG) synthesis but strongly stimulated VLDL-TG secretion, markedly increasing the efficiency of secretion of newly synthesized TG. PGC-1alpha overexpression increased the rate of secretion of apoB100 and promoted secretion of larger, less dense VLDL particles. PGC-1alpha overexpression in intact mouse liver also stimulated rates of VLDL TG secretion and attenuated hepatic TG accumulation resulting from high fat diet feeding. To determine the molecular mechanisms mediating the effect of PGC-1alpha on VLDL assembly, we evaluated the expression of several candidate mediators known to be involved in VLDL assembly or hepatic lipid homeostasis. Cell death-inducing DFFA-like effector B (CideB) expression was greatly induced by PGC-1alpha, and siRNA against CideB reversed the effects of PGC-1alpha on the secretion of TG and VLDL-sized particles by HepG2 cells, indicating that CideB is a critical mediator of stimulatory effects of PGC-1alpha on VLDL secretion. Collectively, these data suggest that PGC-1alpha plays an important role in partitioning cytoplasmic TG toward the VLDL secretory compartments and promoting VLDL secretion via transcriptional induction of CideB.

Indexed as

Transcriptional ActivationAnimalsApoptosis Regulatory ProteinsCell CompartmentationCytoplasmHeat-Shock ProteinsHep G2 CellsHumansLipoproteins, VLDLLiverMicePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaTranscription FactorsTriglyceridesApoptosis Regulatory ProteinsCIDEB protein, humanHeat-Shock ProteinsLipoproteins, VLDLPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanTranscription FactorsTriglyceridesvery low density lipoprotein triglyceride

Identifiers

PMID20551328
PMCPMC2923994
OpenAlexW2054748608

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.