Evidence map›Paper›PMID 34543263›Full record

ArticlePLoS genetics2021

Endothelial lipase mediates efficient lipolysis of triglyceride-rich lipoproteins.

Sumeet A Khetarpal, Cecilia Vitali, Michael G Levin, Derek Klarin, Joseph Park, Akhil Pampana, John S Millar, Takashi Kuwano, Dhavamani Sugasini, Papasani V Subbaiah and 3 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

32 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. ApoJ regulates endothelial lipase activity and stability.Protein science : a publication of the Protein Society · 2026
    Article
  6. Endothelial Cell Regulation of Lipid Uptake During Feeding and Fasting.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Frontiers in cardiovascular medicine · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Article
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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

13 authors at 5 institutions in 1 country.

Sumeet A KhetarpalDepartments of Medicine and Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Cecilia VitaliDepartments of Medicine and Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.ORCID 0000-0002-4519-0798
Michael G LevinDivision of Cardiovascular Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.ORCID 0000-0002-9937-9932
Derek KlarinBoston VA Healthcare System, Boston, Massachusetts, United States of America.ORCID 0000-0002-4636-5780
Joseph ParkDepartments of Medicine and Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.ORCID 0000-0002-3313-641X
Akhil PampanaCardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts, United States of America.ORCID 0000-0002-4167-0540
John S MillarDepartment of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Takashi KuwanoDepartments of Medicine and Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.ORCID 0000-0003-3811-0566
Dhavamani SugasiniSection of Endocrinology, Department of Medicine, University of Illinois at Chicago; Jesse Brown VA Medical Center, Chicago, Illinois, United States of America.ORCID 0000-0001-9077-9940
Papasani V SubbaiahSection of Endocrinology, Department of Medicine, University of Illinois at Chicago; Jesse Brown VA Medical Center, Chicago, Illinois, United States of America.ORCID 0000-0002-9376-8582
Jeffrey T BillheimerDepartment of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Pradeep NatarajanCardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts, United States of America.ORCID 0000-0001-8402-7435
Daniel J RaderDepartments of Medicine and Genetics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.ORCID 0000-0002-9245-9876
University of Pennsylvania · USBroad Institute · USUniversity of Illinois Chicago · USMassachusetts General Hospital · USPhiladelphia VA Medical Center · US

Funding

HDL metabolism: Influence of extracellular lipasesR37HL055323 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI RADER, DANIEL JAMES · 2009 to 2018
$4.0M
High Density Lipoprotein Metabolism Influence of Extracellular PhospholipasesR01HL055323 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI RADER, DANIEL JAMES · 1996 to 2009
$3.0M
ApoC-III: Structure-Function and Regulation of Triglyceride MetabolismF30HL124967 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI KHETARPAL, SUMEET · 2014 to 2016
$123k
BLRD VA I01 BX004315NHLBI NIH HHS F30 HL124967NHLBI NIH HHS R01 HL055323NHLBI NIH HHS R37 HL055323
6 · The paper itself

Abstract

Triglyceride-rich lipoproteins (TRLs) are circulating reservoirs of fatty acids used as vital energy sources for peripheral tissues. Lipoprotein lipase (LPL) is a predominant enzyme mediating triglyceride (TG) lipolysis and TRL clearance to provide fatty acids to tissues in animals. Physiological and human genetic evidence support a primary role for LPL in hydrolyzing TRL TGs. We hypothesized that endothelial lipase (EL), another extracellular lipase that primarily hydrolyzes lipoprotein phospholipids may also contribute to TRL metabolism. To explore this, we studied the impact of genetic EL loss-of-function on TRL metabolism in humans and mice. Humans carrying a loss-of-function missense variant in LIPG, p.Asn396Ser (rs77960347), demonstrated elevated plasma TGs and elevated phospholipids in TRLs, among other lipoprotein classes. Mice with germline EL deficiency challenged with excess dietary TG through refeeding or a high-fat diet exhibited elevated TGs, delayed dietary TRL clearance, and impaired TRL TG lipolysis in vivo that was rescued by EL reconstitution in the liver. Lipidomic analyses of postprandial plasma from high-fat fed Lipg-/- mice demonstrated accumulation of phospholipids and TGs harboring long-chain polyunsaturated fatty acids (PUFAs), known substrates for EL lipolysis. In vitro and in vivo, EL and LPL together promoted greater TG lipolysis than either extracellular lipase alone. Our data positions EL as a key collaborator of LPL to mediate efficient lipolysis of TRLs in humans and mice.

Indexed as

LipolysisAnimalsDiet, High-FatHumansLipaseLipoproteinsLiposomesMiceMutation, MissensePostprandial PeriodTriglyceridesLipaseLIPG protein, humanLipg protein, mouseLipoproteinslipoprotein triglycerideLiposomesTriglycerides

Identifiers

PMID34543263
PMCPMC8483387
OpenAlexW3200189829

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.