Evidence map›Paper›PMID 27582133›Full record

ArticleBMC musculoskeletal disorders2016

Influence of high glucose and advanced glycation end-products (ages) levels in human osteoblast-like cells gene expression.

Cristina Miranda, Mercè Giner, M José Montoya, M Angeles Vázquez, M José Miranda, Ramón Pérez-Cano

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC musculoskeletal disorders, 2016. 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
1.7field-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, 40 citations in OpenAlex.

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  15. Sclerostin Regulation, Microarchitecture, and Advanced Glycation End-Products in the Bone of Elderly Women With Type 2 Diabetes.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020
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  18. Macrophage Control of Incipient Bone Formation in Diabetic Mice.Frontiers in cell and developmental biology · 2020
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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

6 authors at 2 institutions in 1 country.

Cristina MirandaBone Metabolism Unit, Internal Medicine Department, Virgen Macarena University Hospital, Dr. Fedriani s/n, 41009, Seville, Spain.
Mercè GinerBone Metabolism Unit, Internal Medicine Department, Virgen Macarena University Hospital, Dr. Fedriani s/n, 41009, Seville, Spain.
M José MontoyaMedicine Department, University of Seville, Dr. Fedriani s/n, 41009, Seville, Spain. pmontoya@us.es.
M Angeles VázquezMedicine Department, University of Seville, Dr. Fedriani s/n, 41009, Seville, Spain.
M José MirandaBone Metabolism Unit, Internal Medicine Department, Virgen Macarena University Hospital, Dr. Fedriani s/n, 41009, Seville, Spain.
Ramón Pérez-CanoBone Metabolism Unit, Internal Medicine Department, Virgen Macarena University Hospital, Dr. Fedriani s/n, 41009, Seville, Spain.
Hospital Universitario Virgen Macarena · ESUniversidad de Sevilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundType 2 diabetes mellitus (T2DM) is associated with an increased risk of osteoporotic fracture. Several factors have been identified as being potentially responsible for this risk, such as alterations in bone remodelling that may have been induced by changes in circulating glucose or/and by the presence of non-oxidative end products of glycosylation (AGEs). The aim of this study is to assess whether such variations generate a change in the gene expression related to the differentiation and osteoblast activity (OPG, RANKL, RUNX2, OSTERIX, and AGE receptor) in primary cultures of human osteoblast-like cells (hOB).

methodsWe recruited 32 patients; 10 patients had osteoporotic hip fractures (OP group), 12 patients had osteoporotic hip fractures with T2DM (T2DM group), and 10 patients had hip osteoarthritis (OA group) with no osteoporotic fractures and no T2DM. The gene expression was analyzed in hOB cultures treated with physiological glucose concentration (4.5 mM) as control, high glucose (25 mM), and high glucose plus AGEs (2 μg/ml) for 24 h.

resultsThe hOB cultures from patients with hip fractures presented slower proliferation. Additionally, the hOB cultures from the T2DM group were the most negatively affected with respect to RUNX2 and OSX gene expression when treated solely with high glucose or with high glucose plus AGEs. Moreover, high levels of glucose induced a major decrease in the RANKL/OPG ratio when comparing the OP and the T2DM groups to the OA group.

conclusionsOur data indicates an altered bone remodelling rate in the T2DM group, which may, at least partially, explain the reduced bone strength and increased incidence of non-traumatic fractures in diabetic patients.

Indexed as

Bone RemodelingAgedAged, 80 and overBiomarkersBone and BonesCore Binding Factor Alpha 1 SubunitDiabetes Mellitus, Type 2FemaleGene ExpressionGlucoseGlycation End Products, AdvancedHip FracturesHumansMaleOsteoarthritis, HipOsteoblastsBiomarkersCore Binding Factor Alpha 1 SubunitGlucoseGlycation End Products, AdvancedOsteoprotegerinRANK LigandRUNX2 protein, humanSP7 protein, humanSp7 Transcription FactorTNFSF11 protein, human

Identifiers

PMID27582133
PMCPMC5007697
OpenAlexW2507132169

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.