Evidence map›Paper›PMID 37824203›Full record

ArticleThe Journal of clinical investigation2023

Hypertriglyceridemia in Apoa5-/- mice results from reduced amounts of lipoprotein lipase in the capillary lumen.

Ye Yang, Anne P Beigneux, Wenxin Song, Le Phuong Nguyen, Hyesoo Jung, Yiping Tu, Thomas A Weston, Caitlyn M Tran, Katherine Xie, Rachel G Yu and 14 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.7field-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

16 citing papers in PubMed, 17 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. A neutralizing APOA5 monoclonal antibody reduces amounts of lipoprotein lipase in capillaries and triggers hypertriglyceridemia.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Article
  10. Article
  11. ANGPTL3/8 is an atypical unfoldase that regulates intravascular lipolysis by catalyzing unfolding of lipoprotein lipase.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Review
  13. Review
  14. A unified model for regulating lipoprotein lipase activity.Trends in endocrinology and metabolism: TEM · 2024
    Review
  15. Carboxyl-terminal sequences in APOA5 are important for suppressing ANGPTL3/8 activity.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  16. Article
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

24 authors at 5 institutions in 3 countries.

Ye YangDepartment of Medicine and.
Anne P BeigneuxDepartment of Medicine and.
Wenxin SongDepartment of Medicine and.
Le Phuong NguyenDepartment of Medicine and.
Hyesoo JungDepartment of Medicine and.
Yiping TuDepartment of Medicine and.
Thomas A WestonDepartment of Medicine and.
Caitlyn M TranDepartment of Medicine and.
Katherine XieDepartment of Medicine and.
Rachel G YuDepartment of Medicine and.
Anh P TranDepartment of Medicine and.
Kazuya MiyashitaDepartment of Clinical Laboratory Medicine, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Katsuyuki NakajimaDepartment of Clinical Laboratory Medicine, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Masami MurakamiDepartment of Clinical Laboratory Medicine, Gunma University, Graduate School of Medicine, Maebashi, Gunma, Japan.
Yan Q ChenLilly Research Laboratories, Eli Lilly and Company, Indianapolis, Indiana, USA.
Eugene Y ZhenLilly Research Laboratories, Eli Lilly and Company, Indianapolis, Indiana, USA.
Joonyoung R KimDepartment of Medicine and.
Paul H KimDepartment of Medicine and.
Gabriel BirraneDivision of Experimental Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.
Peter TontonozDepartment of Pathology and Laboratory Medicine, UCLA, Los Angeles, California, USA.
Michael PlougFinsen Laboratory, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark.
Robert J KonradLilly Research Laboratories, Eli Lilly and Company, Indianapolis, Indiana, USA.
Loren G FongDepartment of Medicine and.
Stephen G YoungDepartment of Medicine and.
University of California, Los Angeles · USEli Lilly (United States) · USGunma University · JPBeth Israel Deaconess Medical Center · USUniversity of Copenhagen · DK

Funding

The Lipin Protein Family and Triglyceride Metabolism P01HL090553 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2008 to 2018
$23.3M
Understanding the Influence of Lipid Homeostasis on T cell FunctionP01HL146358 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2019 to 2023
$11.7M
Refining Physiologic Mechanisms for Intravascular Triglyceride MetabolismR01HL087228 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BEIGNEUX, ANNE, FONG, LOREN GI · 2007 to 2024
$7.8M
Vascular Biology Training GrantT32HL069766 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LUSIS, ALDONS JAKE · 2002 to 2022
$7.4M
Investigating Mechanisms for Lipid Transport in Health and DiseaseR35HL139725 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YOUNG, STEPHEN G. · 2018 to 2024
$6.1M
Systems Genetics Dissection of Non-alcoholic SteatohepatitisR01DK117850 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Aldons Jake Lusis · 2019 to 2026
$4.6M
Solving longstanding mysteries in plasma triglyceride metabolismR01HL171737 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ANNE BEIGNEUX, Loren Gi Fong · 2024 to 2026
$1.9M
NHLBI NIH HHS P01 HL090553NHLBI NIH HHS P01 HL146358NHLBI NIH HHS R01 HL087228NHLBI NIH HHS R01 HL171737NHLBI NIH HHS R35 HL139725NHLBI NIH HHS T32 HL069766NIDDK NIH HHS R01 DK117850
6 · The paper itself

Abstract

Why apolipoprotein AV (APOA5) deficiency causes hypertriglyceridemia has remained unclear, but we have suspected that the underlying cause is reduced amounts of lipoprotein lipase (LPL) in capillaries. By routine immunohistochemistry, we observed reduced LPL staining of heart and brown adipose tissue (BAT) capillaries in Apoa5-/- mice. Also, after an intravenous injection of LPL-, CD31-, and GPIHBP1-specific mAbs, the binding of LPL Abs to heart and BAT capillaries (relative to CD31 or GPIHBP1 Abs) was reduced in Apoa5-/- mice. LPL levels in the postheparin plasma were also lower in Apoa5-/- mice. We suspected that a recent biochemical observation - that APOA5 binds to the ANGPTL3/8 complex and suppresses its capacity to inhibit LPL catalytic activity - could be related to the low intracapillary LPL levels in Apoa5-/- mice. We showed that an ANGPTL3/8-specific mAb (IBA490) and APOA5 normalized plasma triglyceride (TG) levels and intracapillary LPL levels in Apoa5-/- mice. We also showed that ANGPTL3/8 detached LPL from heparan sulfate proteoglycans and GPIHBP1 on the surface of cells and that the LPL detachment was blocked by IBA490 and APOA5. Our studies explain the hypertriglyceridemia in Apoa5-/- mice and further illuminate the molecular mechanisms that regulate plasma TG metabolism.

Indexed as

Apolipoprotein A-VHypertriglyceridemiaReceptors, LipoproteinAnimalsCapillariesLipoprotein LipaseMiceTriglyceridesApoa5 protein, mouseApolipoprotein A-VLipoprotein LipaseReceptors, LipoproteinTriglyceridesEndothelial cellsLipoproteinsMetabolismMouse modelsVascular Biology

Identifiers

PMID37824203
PMCPMC10688983
OpenAlexW4387580731

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.