Evidence map›Paper›PMID 25568062›Full record

Trial reportJournal of lipid research2015

Ext1 heterozygosity causes a modest effect on postprandial lipid clearance in humans.

Hans L Mooij, Sophie J Bernelot Moens, PhilipL S M Gordts, KristinI Stanford, ErinM Foley, MarjoleinA W van den Boogert, JuliaJ Witjes, H Carlijne Hassing, MichaelW Tanck, MichielA J van de Sande and 6 more

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

19 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
  3. Osteochondroma formation is independent of heparanase expression as revealed in a mouse model of hereditary multiple exostoses.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. The heparan sulfate proteoglycan grip on hyperlipidemia and atherosclerosis.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Review
  13. The pathogenic roles of heparan sulfate deficiency in hereditary multiple exostoses.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Hereditary Multiple Exostoses: a review of clinical appearance and metabolic pattern.Clinical cases in mineral and bone metabolism : the official journal of the Italian Society of Osteoporosis, Mineral Metabolism, and Skeletal Diseases
    Review
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

16 authors at 3 institutions in 2 countries.

Hans L MooijDepartment of Vascular Medicine.
Sophie J Bernelot MoensDepartment of Vascular Medicine.
PhilipL S M GordtsDepartment of Cellular and Molecular Medicine, University of California San Diego, San Diego, CA.
KristinI StanfordDepartment of Cellular and Molecular Medicine, University of California San Diego, San Diego, CA.
ErinM FoleyDepartment of Cellular and Molecular Medicine, University of California San Diego, San Diego, CA.
MarjoleinA W van den BoogertDepartment of Vascular Medicine.
JuliaJ WitjesDepartment of Vascular Medicine.
H Carlijne HassingDepartment of Vascular Medicine.
MichaelW TanckDepartment of Clinical Epidemiology, Biostatistics and Bioinformatics.
MichielA J van de SandeDepartment of Orthopedics, Leiden University Medical Center, Leiden, the Netherlands.
J Han LevelsDepartment of Experimental Vascular Medicine, Academic Medical Center, Amsterdam, the Netherlands.
JohnJ P KasteleinDepartment of Vascular Medicine.
ErikS G StroesDepartment of Vascular Medicine.
GeesjeM Dallinga-ThieDepartment of Vascular Medicine; Department of Experimental Vascular Medicine, Academic Medical Center, Amsterdam, the Netherlands.
JeffD EskoDepartment of Cellular and Molecular Medicine, University of California San Diego, San Diego, CA.
Max NieuwdorpDepartment of Vascular Medicine; Department of Experimental Vascular Medicine, Academic Medical Center, Amsterdam, the Netherlands. Electronic address: m.nieuwdorp@amc.uva.nl.
University of California, San Diego · USAcademic Medical Center · NLLeiden University Medical Center · NL

Funding

Siglec Modulation of Inflammation in Humans and MiceP01HL057345 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LE, DZUNG T · 1997 to 2012
$24.1M
GENETIC CONTROL OF PROTEOGLYCAN METABOLISMR37GM033063 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ESKO, JEFFREY D · 2000 to 2010
$3.9M
LIPID METABOLISM IN ANIMAL CELLSR01GM033063 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ESKO, JEFFREY D · 1985 to 2019
$3.4M
Drug Discovery for Multiple Hereditary ExostosesR01AR064202 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ESKO, JEFFREY D · 2013 to 2017
$1.9M
NHLBI NIH HHS HL57345NHLBI NIH HHS P01 HL057345NIAMS NIH HHS R01 AR064202NIGMS NIH HHS GM33063NIGMS NIH HHS R01 GM033063NIGMS NIH HHS R37 GM033063
6 · The paper itself

Abstract

Elevated nonfasting TG-rich lipoprotein levels are a risk factor for CVD. To further evaluate the relevance of LDL-receptor (LDLr) pathway and heparan sulfate proteoglycans (HSPGs) in TG homeostasis, we analyzed fasting and postprandial TG levels in mice bearing combined heterozygous mutations in both Exostosin (Ext) 1 and Ldlr, in subjects with hereditary multiple exostosis (HME) due to a heterozygous loss-of-function mutation in EXT1 or EXT2 (N = 13), and in patients with heterozygous mutations in LDLR [familial hypercholesterolemia (FH)] and SNPs in major HSPG-related genes (n = 22). Mice bearing a homozygous mutation in hepatic Ext1 exhibited elevated plasma TGs similar to mice lacking other key enzymes involved in HSPG assembly. Compound heterozygous mice lacking Ldlr and Ext1 showed synergy on plasma TG accumulation and postprandial clearance. In human subjects, a trend was observed in HME patients toward reduced postprandial TG clearance with a concomitant reduction in chylomicron clearance [area under the curve (AUC)-retinyl ester (RE) HME, 844 ± 127 vs. controls, 646 ± 119 nM/h, P = 0.09]. Moreover, in FH subjects with a high HSPG gene score, retinyl palmitate excursions were higher (AUC-RE, 2,377 ± 293 vs. 1,565 ± 181 nM/h, P < 0.05). Incremental AUC-apoB48 was similar between the groups. In conclusion, the data are supportive for a minor yet additive role of HSPG in human postprandial TG clearance, and further studies are warranted.

Indexed as

HeterozygoteMultiple SclerosisMutationN-AcetylglucosaminyltransferasesPostprandial PeriodTriglyceridesAdultAnimalsExostosin 1Exostosin 2FemaleHumansMaleMiceMice, KnockoutMiddle AgedExostosin 1Exostosin 2N-AcetylglucosaminyltransferasesTriglyceridesfamilial hypercholesterolemiaheparan sulfateshereditary multiple exostosestriglycerides

Identifiers

PMID25568062
PMCPMC4340313
OpenAlexW2319630805

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.