Evidence map›Paper›PMID 18160395›Full record

ArticleThe Journal of biological chemistry2008

Apolipoprotein AII is a regulator of very low density lipoprotein metabolism and insulin resistance.

Lawrence W Castellani, Cara N Nguyen, Sarada Charugundla, Michael M Weinstein, Chau X Doan, William S Blaner, Nuttaporn Wongsiriroj, Aldons J Lusis

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

40 citing papers in PubMed, 80 citations in OpenAlex.

  1. p21Nature aging · 2026
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  18. Proteomic analysis to identify candidate biomarkers associated with type 1 diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2018
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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

8 authors at 2 institutions in 1 country.

Lawrence W CastellaniDepartments of Medicine/Cardiology University of California, Los Angeles, Los Angeles, California 90095, USA. lcastellani@mednet.ucla.edu
Cara N Nguyen
Sarada Charugundla
Michael M Weinstein
Chau X Doan
William S Blaner
Nuttaporn Wongsiriroj
Aldons J Lusis
University of California, Los Angeles · USColumbia University · US

Funding

Systems genomics of metabolic syndrome traitsP01HL028481 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI REUE, KAREN · 1985 to 2019
$50.2M
Genetic Analysis of the Diabetes-Prone C57BLKS StrainR01DK071673 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2005 to 2009
$1.6M
NHLBI NIH HHS HL28481NIDDK NIH HHS DK071673
6 · The paper itself

Abstract

Apolipoprotein AII (apoAII) transgenic (apoAIItg) mice exhibit several traits associated with the insulin resistance (IR) syndrome, including IR, obesity, and a marked hypertriglyceridemia. Because treatment of the apoAIItg mice with rosiglitazone ameliorated the IR and hypertriglyceridemia, we hypothesized that the hypertriglyceridemia was due largely to overproduction of very low density lipoprotein (VLDL) by the liver, a normal response to chronically elevated insulin and glucose. We now report in vivo and in vitro studies that indicate that hepatic fatty acid oxidation was reduced and lipogenesis increased, resulting in a 25% increase in triglyceride secretion in the apoAIItg mice. In addition, we observed that hydrolysis of triglycerides from both chylomicrons and VLDL was significantly reduced in the apoAIItg mice, further contributing to the hypertriglyceridemia. This is a direct, acute effect, because when mouse apoAII was injected into mice, plasma triglyceride concentrations were significantly increased within 4 h. VLDL from both control and apoAIItg mice contained significant amounts of apoAII, with approximately 4 times more apoAII on apoAIItg VLDL. ApoAII was shown to transfer spontaneously from high density lipoprotein (HDL) to VLDL in vitro, resulting in VLDL that was a poorer substrate for hydrolysis by lipoprotein lipase. These results indicate that one function of apoAII is to regulate the metabolism of triglyceride-rich lipoproteins, with HDL serving as a plasma reservoir of apoAII that is transferred to the triglyceride-rich lipoproteins in much the same way as VLDL and chylomicrons acquire most of their apoCs from HDL.

Indexed as

Gene Expression RegulationInsulin ResistanceAnimalsApolipoprotein A-IIChylomicronsDiterpenesFatty AcidsHydrolysisLipoproteins, VLDLLiverMiceMice, Inbred C57BLMice, TransgenicModels, BiologicalRetinyl EstersTriglyceridesApolipoprotein A-IIChylomicronsDiterpenesFatty AcidsLipoproteins, VLDLretinol palmitateRetinyl EstersTriglyceridesVitamin A

Identifiers

PMID18160395
PMCPMC2431075
OpenAlexW2049526812

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.