Evidence map›Paper›PMID 22345169›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

Transgenic expression and genetic variation of Lmf1 affect LPL activity in mice and humans.

Maryam Hosseini, Nicole Ehrhardt, Daphna Weissglas-Volkov, Ching-Mei Lai, Hui Z Mao, Jo-Ling Liao, Elina Nikkola, André Bensadoun, Marja-Riitta Taskinen, Mark H Doolittle and 2 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 18 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

12 authors at 3 institutions in 1 country.

Maryam HosseiniMedical Genetics Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Nicole Ehrhardt
Daphna Weissglas-Volkov
Ching-Mei Lai
Hui Z Mao
Jo-Ling Liao
Elina Nikkola
André Bensadoun
Marja-Riitta Taskinen
Mark H Doolittle
Päivi Pajukanta
Miklós Péterfy
VA Greater Los Angeles Healthcare System · USCornell University · USCedars-Sinai Medical Center · US

Funding

Systems genomics of metabolic syndrome traitsP01HL028481 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 1985 to 2019
$50.2M
Training Grant in Genomic Analysis and InterpretationT32HG002536 · NHGRI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Valerie A Arboleda, Harold Pimentel · 2002 to 2026
$8.6M
Genomics of dyslipidemia in MexicansR01HL095056 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PAJUKANTA, PAIVI · 2009 to 2018
$5.9M
NHGRI NIH HHS T32 HG002536NHLBI NIH HHS HL028481NHLBI NIH HHS HL095056NHLBI NIH HHS P01 HL028481NHLBI NIH HHS R01 HL095056
6 · The paper itself

Abstract

objectiveLipoprotein lipase (LPL) is a principal enzyme in lipoprotein metabolism, tissue lipid utilization, and energy metabolism. LPL is synthesized by parenchymal cells in adipose, heart, and muscle tissues followed by secretion to extracellular sites, where lipolyic function is exerted. The catalytic activity of LPL is attained during posttranslational maturation, which involves glycosylation, folding, and subunit assembly within the endoplasmic reticulum. A lipase-chaperone, lipase maturation factor 1 (Lmf1), has recently emerged as a critical factor in this process. Previous studies demonstrated that loss-of-function mutations of Lmf1 result in diminished lipase activity and severe hypertriglyceridemia in mice and human subjects. The objective of this study is to investigate whether, beyond its role as a required factor in lipase maturation, variation in Lmf1 expression is sufficient to modulate LPL activity in vivo. METHODS AND

resultsTo assess the effects of Lmf1 overexpression in adipose and muscle tissues, we generated aP2-Lmf1 and Mck-Lmf1 transgenic mice. Characterization of relevant tissues revealed increased LPL activity in both mouse strains. In the omental and subcutaneous adipose depots, Lmf1 overexpression was associated with increased LPL specific activity without changes in LPL mass. In contrast, increased LPL activity was due to elevated LPL protein level in heart and gonadal adipose tissue. To extend these studies to humans, we detected association between LMF1 gene variants and postheparin LPL activity in a dyslipidemic cohort.

conclusionsOur results suggest that variation in Lmf1 expression is a posttranslational determinant of LPL activity.

Indexed as

Gene Expression RegulationGenetic VariationAdipose TissueAnimalsDNAEnergy MetabolismHumansHypertriglyceridemiaLipoprotein LipaseMembrane ProteinsMiceMice, TransgenicMuscle, SkeletalMyocardiumDNALipoprotein LipaseLMF1 protein, mouseMembrane Proteins

Identifiers

PMID22345169
PMCPMC3331946
OpenAlexW2166973555

What OpenQuestion holds

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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.