Evidence map›Paper›PMID 29077850›Full record

ArticleEndocrinology2018

β-Catenin Directs Long-Chain Fatty Acid Catabolism in the Osteoblasts of Male Mice.

Julie L Frey, Soohyun P Kim, Zhu Li, Michael J Wolfgang, Ryan C Riddle

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. Skeletal stem cell lineages in osteosarcoma and bone metastasis.Journal of bone and mineral metabolism · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
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

5 authors at 3 institutions in 1 country.

Julie L FreyDepartment of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Soohyun P KimDepartment of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Zhu LiDepartment of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Michael J WolfgangDepartment of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Ryan C RiddleDepartment of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Johns Hopkins University · USJohns Hopkins Medicine · USUnited States Department of Veterans Affairs · US

Funding

JHU-UMD Diabetes Research CenterP30DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI AHIMA, REXFORD S. · 2013 to 2017
$9.7M
Diabetes Research and Training CenterP60DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI WONDISFORD, FREDRIC E. · 2008 to 2012
$9.1M
Regulation of Neuronal Lipid Homeostasis By ThioesterasesR01NS072241 · NINDS · JOHNS HOPKINS UNIVERSITY · PI WOLFGANG, MICHAEL J. · 2011 to 2020
$4.0M
Regulation of Osteoblast Metabolism by Lrp5R01DK099134 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI RIDDLE, RYAN C · 2013 to 2022
$3.4M
NIDDK NIH HHS P30 DK079637NIDDK NIH HHS P60 DK079637NIDDK NIH HHS R01 DK099134NINDS NIH HHS R01 NS072241
6 · The paper itself

Abstract

Wnt-initiated signaling through a frizzled receptor and the low-density lipoprotein-related receptor-5 coreceptor instructs key anabolic events during skeletal development, homeostasis, and repair. Recent studies indicate that Wnt signaling also regulates the intermediary metabolism of osteoblastic cells, inducing glucose consumption in osteoprogenitors and fatty acid utilization in mature osteoblasts. In this study, we examined the role of the canonical Wnt-signaling target, β-catenin, in the control of osteoblast metabolism. In vitro, Wnt ligands and agonists that stimulated β-catenin activation in osteoblasts enhanced fatty acid catabolism, whereas genetic ablation of β-catenin dramatically reduced oleate oxidation concomitant with reduced osteoblast maturation and increased glycolytic metabolism. Temporal ablation of β-catenin expression in osteoblasts in vivo produced the expected low-bone-mass phenotype and also led to an increase in white adipose tissue mass, dyslipidemia, and impaired insulin sensitivity. Because the expression levels of enzymatic mediators of fatty acid β-oxidation are reduced in the skeleton of β-catenin mutants, these results further confirm the role of the osteoblast in lipid metabolism and indicate that the influence of Wnt signaling on fatty acid utilization proceeds via its canonical signaling pathway.

Indexed as

Gene Expression Regulation, DevelopmentalLipid MetabolismWnt Signaling PathwayAdipose Tissue, WhiteAdiposityAnimalsAnimals, Newbornbeta CateninCaloric RestrictionCells, CulturedCrosses, GeneticFatty Acids, NonesterifiedLigandsMaleMice, Inbred C57BLMice, Mutant Strainsbeta CateninCTNNB1 protein, mouseFatty Acids, NonesterifiedLigandsWnt Proteins

Identifiers

PMID29077850
PMCPMC5761587
OpenAlexW2765459461

What OpenQuestion holds

Textmetadata
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.