Evidence map›Paper›PMID 28843700›Full record

ReviewBone2018

Glucose metabolism in bone.

Courtney M Karner, Fanxin Long

Open access · greenAbstract readReview
In one paragraph

Review in Bone, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

106 citing papers in PubMed, 152 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Glucose metabolism in osteoporosis: A potential therapeutic target (Review).International journal of molecular medicine · 2026
    Review
  4. Bone organoids and mitochondrial reprogramming.Journal of orthopaedic translation · 2026
    Review
  5. Extracellular vesicle-mediated crosstalk in bone: miR-150-5p as a mechanosensitive regulator of osteoclastogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  6. Article
  7. Lactate regulates osteoclastogenesis via H3k18la in osteoarthritis.International journal of molecular medicine · 2026
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. METTL14 MediatesRedox report : communications in free radical research · 2025
    Article
  18. Review
  19. Article
  20. Review

46 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Courtney M KarnerDepartment of Orthopaedic Surgery, Duke Orthopaedic Cellular, Developmental, and Genome Laboratories, Department of Cell Biology, Duke University School of Medicine, Durham, NC 27710, USA. Electronic address: courtney.karner@duke.edu.
Fanxin LongDepartment of Orthopaedic Surgery, Department of Developmental Biology, Washington University School of Medicine, St Louis, MO 63131, USA. Electronic address: flong@wustl.edu.
Duke University · USWashington University in St. Louis · US

Funding

Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Jonathan R Brestoff · 1999 to 2026
$30.2M
Mechanisms of WNT Signaling In BoneR01AR060456 · NIAMS · WASHINGTON UNIVERSITY · PI LONG, FANXIN · 2010 to 2020
$4.0M
Notch Signaling and Bone FormationR01AR055923 · NIAMS · WASHINGTON UNIVERSITY · PI LONG, FANXIN · 2008 to 2017
$3.5M
NIAMS NIH HHS R01 AR055923NIAMS NIH HHS R01 AR060456NIDDK NIH HHS P30 DK056341
6 · The paper itself

Abstract

The adult human skeleton is a multifunctional organ undergoing constant remodeling through the opposing activities of the bone-resorbing osteoclast and the bone-forming osteoblast. The exquisite balance between bone resorption and bone formation is responsible for bone homeostasis in healthy adults. However, evidence has emerged that such a balance is likely disrupted in diabetes where systemic glucose metabolism is dysregulated, resulting in increased bone frailty and osteoporotic fractures. These findings therefore underscore the significance of understanding the role and regulation of glucose metabolism in bone under both normal and pathological conditions. Recent studies have shed new light on the metabolic plasticity and the critical functions of glucose metabolism during osteoclast and osteoblast differentiation. Moreover, these studies have begun to identify intersections between glucose metabolism and the growth factors and transcription factors previously known to regulate osteoblasts and osteoclasts. Here we summarize the current knowledge in the nascent field, and suggest that a fundamental understanding of glucose metabolic pathways in the critical bone cell types may open new avenues for developing novel bone therapeutics.

Indexed as

AnimalsBone and BonesBone RemodelingGlucoseHumansOsteoblastsOsteoclastsGlucoseBoneDiabetesGlucoseGlycolysisMetabolismMitochondriaOsteoblastOsteoclastOsteoporosisOxidative phosphorylation (OXPHOS)

Identifiers

PMID28843700
PMCPMC6030501
OpenAlexW2746496668

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.