Evidence map›Paper›PMID 26211993›Full record

ReviewBone2016

Effect of type 2 diabetes-related non-enzymatic glycation on bone biomechanical properties.

Lamya Karim, Mary L Bouxsein

Open access · greenAbstract readReview
In one paragraph

Review in Bone, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
8.9field-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

60 citing papers in PubMed, 121 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Advanced-Glycation Endproducts: How cross-linking properties affect the collagen fibril behavior.Journal of the mechanical behavior of biomedical materials · 2023
    Article
  14. Microstructural fatigue fracture behavior of glycated cortical bone.Medical & biological engineering & computing · 2023
    Article
  15. Review
  16. Article
  17. Relative Effects of Radiation-Induced Changes in Bone Mass, Structure, and Tissue Material on Vertebral Strength in a Rat Model.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023
    Article
  18. The influence of AGEs and enzymatic cross-links on the mechanical properties of collagen fibrils.Journal of the mechanical behavior of biomedical materials · 2023
    Article
  19. Effect of non-enzymatic glycation on collagen nanoscale mechanisms in diabetic and age-related bone fragility.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2023
    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

2 authors at 1 institution in 1 country.

Lamya KarimCenter for Advanced Orthopedic Studies, Beth Israel Deaconess Medical Center, Department of Orthopedic Surgery, Harvard Medical School, Boston, MA 02215 USA. Electronic address: lkarim@bidmc.harvard.edu.
Mary L BouxseinCenter for Advanced Orthopedic Studies, Beth Israel Deaconess Medical Center, Department of Orthopedic Surgery, Harvard Medical School, Boston, MA 02215 USA. Electronic address: mbouxsei@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · US

Funding

Harvard Clinical and Translational Science CenterUL1TR001102 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2013 to 2017
$106.2M
Transgenic CoreP30DK057521 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI FLOREZ, JOSE CARLOS · 2000 to 2019
$31.4M
NCATS NIH HHS UL1 TR001102NIDDK NIH HHS P30 DK057521
6 · The paper itself

Abstract

There is clear evidence that patients with type 2 diabetes mellitus (T2D) have increased fracture risk, despite having high bone mineral density (BMD) and body mass index (BMI). Thus, poor bone quality has been implicated as a mechanism contributing to diabetic skeletal fragility. Poor bone quality in T2D may result from the accumulation of advanced glycation end-products (AGEs), which are post-translational modifications of collagen resulting from a spontaneous reaction between extracellular sugars and amino acid residues on collagen fibers. This review discusses what is known and what is not known regarding AGE accumulation and diabetic skeletal fragility, examining evidence from in vitro experiments to simulate a diabetic state, ex vivo studies in normal and diabetic human bone, and diabetic animal models. Key findings in the literature are that AGEs increase with age, affect bone cell behavior, and are altered with changes in bone turnover. Further, they affect bone mechanical properties and microdamage accumulation, and can be inhibited in vitro by various inhibitors and breakers (e.g. aminoguanidine, N-Phenacylthiazolium Bromide, vitamin B6). While a few studies report higher AGEs in diabetic animal models, there is little evidence of AGE accumulation in bone from diabetic patients. There are several limitations and inconsistencies in the literature that should be noted and studied in greater depth including understanding the discrepancies between glycation levels across reported studies, clarifying differences in AGEs in cortical versus cancellous bone, and improving the very limited data available regarding glycation content in diabetic animal and human bone, and its corresponding effect on bone material properties in T2D.

Indexed as

AnimalsBiomechanical PhenomenaBone DensityDiabetes Mellitus, Type 2Fractures, BoneGlycation End Products, AdvancedHumansOsteoporosisGlycation End Products, AdvancedAdvanced glycation end-productsBone mechanicsBone qualityBone strengthDiabetes

Identifiers

PMID26211993
PMCPMC4679472
OpenAlexW959211720

What OpenQuestion holds

Textmetadata
LicenceTDM
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.