Evidence map›Paper›PMID 26418133›Full record

ArticlePloS one2015

Osteodystrophy in Cholestatic Liver Diseases Is Attenuated by Anti-γ-Glutamyl Transpeptidase Antibody.

Yusuke Kawazoe, Mutsumi Miyauchi, Atsuhiro Nagasaki, Hisako Furusho, Syunryo Yanagisawa, Chea Chanbora, Toshihiro Inubushi, Hideyuki Hyogo, Takashi Nakamoto, Keiko Suzuki and 4 more

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

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

2 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review: Pathogenesis of cholestatic liver diseases.World journal of hepatology · 2020
    Review
  2. 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

14 authors at 4 institutions in 1 country.

Yusuke KawazoeDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Mutsumi MiyauchiDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Atsuhiro NagasakiDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Hisako FurushoDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Syunryo YanagisawaDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Chea ChanboraDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Toshihiro InubushiDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Hideyuki HyogoDepartment of Medicine and Molecular Science, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Takashi NakamotoDepartment of Oral and Maxillofacial Radiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Keiko SuzukiDepartment of Pharmacology, School of Dentistry, Showa University, Tokyo, Japan.
Sawako MoriwakiBiobank Omics Unit, National Center for Geriatrics and Gerontology, Aichi, Japan.
Susumu TazumaDepartments of General Internal Medicine, Hiroshima University Hospital, Hiroshima, Japan.
Shumpei NiidaBiobank Omics Unit, National Center for Geriatrics and Gerontology, Aichi, Japan.
Takashi TakataDepartment of Oral and Maxillofacial Pathobiology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Hiroshima University · JPNational Center for Geriatrics and Gerontology · JPHiroshima University Hospital · JPShowa University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCholestatic liver diseases exhibit higher levels of serum γ-glutamyl transpeptidase (GGT) and incidence of secondary osteoporosis. GGT has been identified as a novel bone-resorbing factor that stimulates osteoclast formation. The aim of this study was to elucidate the interaction of elevated GGT levels and cholestatic liver disease-induced bone loss.

methodsWistar rats were divided into three groups: sham-operated control (SO) rats, bile duct ligation (BDL) rats, and anti-GGT antibody-treated BDL rats (AGT). Serum GGT level was measured. Bone mineral density (BMD) was analyzed by dual-energy X-ray absorptiometry. Bone morphometric parameters and microarchitectural properties were determined by micro-computed tomography and histomorphometry of the distal metaphysis of femurs. Alterations of bone metabolism-related factors were evaluated by cytokine array. Effects of GGT on osteoblasts or stromal cells were evaluated by RT-PCR, enzyme activity, and mineralization ability.

resultsSerum levels of GGT were significantly elevated in the BDL-group. In the BDL group, BMD, bone mass percentage, and osteoblast number were significantly decreased, whereas osteoclast number was significantly increased. These alterations were markedly attenuated in the AGT group. The mRNA levels of vascular endothelial growth factor-A, LPS-induced CXC chemokine, monocyte chemoattractant protein-1, tumor necrosis factor-α interleukin-1β and receptor activator of nuclear factor-kappa B ligand were upregulated, and those of interferon-γ and osteoprotegerin were downregulated in the GGT-treated stromal cells. Furthermore, GGT inhibited mineral nodule formation and expression of alkaline phosphatase and bone sialo-protein in osteoblastic cells.

conclusionOur results indicate that elevated GGT level is involved in hepatic osteodystrophy through secretion of bone resorbing factor from GGT-stimulated osteoblasts/bone marrow stromal cells. In addition, GGT also possesses suppressive effects on bone formation. Managing elevated GGT levels by anti-GGT antibody may become a novel therapeutic agent for hepatic osteodystrophy in chronic liver diseases.

Indexed as

Absorptiometry, PhotonAnimalsAnimals, NewbornAntibodies, MonoclonalBile DuctsBlotting, WesternBone and BonesBone DensityBone Diseases, MetabolicCell DifferentiationCells, CulturedCholestasisgamma-GlutamyltransferaseGene ExpressionHumansLigationAntibodies, Monoclonalgamma-GlutamyltransferaseRecombinant Proteins

Identifiers

PMID26418133
PMCPMC4587927
OpenAlexW2194528189

What OpenQuestion holds

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LicenceCC BY
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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.