Evidence map›Paper›PMID 23000317›Full record

ReviewClinical biochemistry2013

The paradox of ApoA5 modulation of triglycerides: evidence from clinical and basic research.

Mahdi Garelnabi, Kenton Lor, Jun Jin, Fei Chai, Nalini Santanam

Open access · greenAbstract readReview
In one paragraph

Review in Clinical biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
4.2field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 77 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Mahdi GarelnabiDepartment of Clinical Laboratory and Nutritional Sciences, University of Massachusetts Lowell, MA 01854, USA. Mahdi_Garelnabi@uml.edu
Kenton Lor
Jun Jin
Fei Chai
Nalini Santanam
University of Massachusetts Lowell · USMarshall University · US

Funding

WV INBRE: The Inhibitor of Growth Family Member 4 (ING4) inhibits L-Type Amino Acid Transporter 1 (LAT1) expression to suppress Breast CancerP20GM103434 · NIGMS · MARSHALL UNIVERSITY · PI Travis Salisbury · 2012 to 2026
$61.1M
WVU &MU NEW FACULTY GRANTSP20RR016477 · NCRR · MARSHALL UNIVERSITY · PI RANKIN, GARY O · 2001 to 2011
$35.5M
Oxidized Lipids in Cardiovascular DiseaseR01HL074239 · NHLBI · MARSHALL UNIVERSITY · PI SANTANAM, NALINI · 2004 to 2008
$1.8M
NCRR NIH HHS P20 RR016477NCRR NIH HHS P20RR016477NHLBI NIH HHS R01 HL074239NIGMS NIH HHS P20 GM103434NIGMS NIH HHS P20GM103434
6 · The paper itself

Abstract

unlabelledApolipoprotein A5 (ApoA5) is a key regulator of plasma triglycerides (TG), even though its plasma concentration is very low compared to other known apoproteins. Over the years, researchers have attempted to elucidate the molecular mechanisms by which ApoA5 regulates plasma TG in vivo. Though still under debate, two theories broadly describe how ApoA5 modulates TG levels: (i) ApoA5 enhances the catabolism of TG-rich lipoproteins and (ii) it inhibits the rate of production of very low-density lipoprotein (VLDL), the major carrier of TGs. This review will summarize the basic and clinical studies that describe the importance of ApoA5 in TG metabolism. Population studies conducted in various countries have demonstrated an association between single nucleotide polymorphisms (SNPs) in ApoA5 and the increased risk to cardiovascular disease and metabolic syndrome (including diabetes and obesity). ApoA5 is also highly expressed during liver regeneration and is an acute phase protein associated with HDL, which is independent of its effects on TG metabolism.

conclusionDespite considerable evidences available from clinical and basic research studies on the role of ApoA5 in TG metabolism and its indirect link to metabolic diseases, additional investigations are needed to understand the paradoxical role of this important apoprotein is modulated by both diet and its polymorphism variants.

Indexed as

Polymorphism, Single NucleotideAnimalsApolipoprotein A-VApolipoproteins ACardiovascular DiseasesDiabetes MellitusDietGenetic Predisposition to DiseaseHumansMetabolic SyndromeObesityTriglyceridesAPOA5 protein, humanApolipoprotein A-VApolipoproteins ATriglycerides

Identifiers

PMID23000317
PMCPMC3534811
OpenAlexW1969830206

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.