Evidence map›Paper›PMID 16207378›Full record

ArticleCardiovascular diabetology2005

Distinct effects of glucose and glucosamine on vascular endothelial and smooth muscle cells: evidence for a protective role for glucosamine in atherosclerosis.

Wenlan Duan, Latha Paka, Sivaram Pillarisetti

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  7. Review
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  9. Article
  10. Review
  11. ProteinFrontiers in endocrinology · 2018
    Review
  12. Shear-induced endothelial NOS activation and remodeling via heparan sulfate, glypican-1, and syndecan-1.Integrative biology : quantitative biosciences from nano to macro · 2014
    Article
  13. Hyperglycemia induces altered expressions of angiogenesis associated molecules in the trophoblast.Evidence-based complementary and alternative medicine : eCAM · 2013
    Article
  14. Use of glucosamine and chondroitin in relation to mortality.European journal of epidemiology · 2012
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Total mortality risk in relation to use of less-common dietary supplements.The American journal of clinical nutrition · 2010
    Article
  20. 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

3 authors at 2 institutions in 1 country.

Wenlan DuanReddy US therapeutics, 3065 Northwoods Circle, Norcross, GA 30071, USA. wduan@reddyus.com
Latha Paka
Sivaram Pillarisetti
Angion (United States) · USNorthwell Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accelerated atherosclerosis is one of the major vascular complications of diabetes. Factors including hyperglycemia and hyperinsulinemia may contribute to accelerated vascular disease. Among the several mechanisms proposed to explain the link between hyperglycemia and vascular dysfunction is the hexosamine pathway, where glucose is converted to glucosamine. Although some animal experiments suggest that glucosamine may mediate insulin resistance, it is not clear whether glucosamine is the mediator of vascular complications associated with hyperglycemia. Several processes may contribute to diabetic atherosclerosis including decreased vascular heparin sulfate proteoglycans (HSPG), increased endothelial permeability and increased smooth muscle cell (SMC) proliferation. In this study, we determined the effects of glucose and glucosamine on endothelial cells and SMCs in vitro and on atherosclerosis in apoE null mice. Incubation of endothelial cells with glucosamine, but not glucose, significantly increased matrix HSPG (perlecan) containing heparin-like sequences. Increased HSPG in endothelial cells was associated with decreased protein transport across endothelial cell monolayers and decreased monocyte binding to subendothelial matrix. Glucose increased SMC proliferation, whereas glucosamine significantly inhibited SMC growth. The antiproliferative effect of glucosamine was mediated via induction of perlecan HSPG. We tested if glucosamine affects atherosclerosis development in apoE-null mice. Glucosamine significantly reduced the atherosclerotic lesion in aortic root. (P < 0.05) These data suggest that macrovascular disease associated with hyperglycemia is unlikely due to glucosamine. In fact, glucosamine by increasing HSPG showed atheroprotective effects.

Indexed as

AnimalsAortaApolipoproteins EAtherosclerosisBiological TransportCattleCell DivisionCell Membrane PermeabilityEndothelial CellsGlucosamineGlucoseGlycosaminoglycansHeparan Sulfate ProteoglycansHeparinLipoproteins, LDLMaleApolipoproteins EGlucosamineGlucoseGlycosaminoglycansHeparan Sulfate ProteoglycansHeparinLipoproteins, LDLperlecanSulfates

Identifiers

PMID16207378
PMCPMC1277831
OpenAlexW2131796098

What OpenQuestion 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 OpenQuestion graph.