Evidence map›Paper›PMID 21113585›Full record

ReviewCalcified tissue international2011

The role of GH/IGF-I-mediated mechanisms in sex differences in cortical bone size in mice.

Lisa E Olson, Claes Ohlsson, Subburaman Mohan

Abstract readReview
In one paragraph

Review in Calcified tissue international, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Sex steroid actions in male bone.Endocrine reviews · 2014
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Causes, consequences, and treatment of osteoporosis in men.Drug design, development and therapy · 2013
    Review
  15. Pamidronate for the treatment of osteoporosis secondary to chronic cholestatic liver disease in Wistar rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2012
    Article
  16. Review
  17. Article
  18. 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

3 authors at 3 institutions in 2 countries.

Lisa E OlsonMusculoskeletal Disease Center, Jerry L. Pettis Memorial VA Medical Center and Loma Linda University, Loma Linda, CA 92357, USA.
Claes Ohlsson
Subburaman Mohan
Jerry L. Pettis Memorial VA Medical Center · USLoma Linda University · USUniversity of Gothenburg · SE

Funding

Transgenic Approaches to Evaluate IGF-I Role in Peak BMDR01AR048139 · NIAMS · LOMA LINDA VETERANS ASSN RESEARCH &EDUC · PI MOHAN, SUBBURAMAN · 2003 to 2025
$4.7M
Transgenic Approaches to Evalute IGF-1 Role in Peak BMDR56AR048139 · NIAMS · LOMA LINDA VETERANS ASSN RESEARCH & EDUC · PI MOHAN, SUBBURAMAN · 2008 to 2008
$258k
NIAMS NIH HHS AR48139NIAMS NIH HHS R01 AR048139NIAMS NIH HHS R56 AR048139
6 · The paper itself

Abstract

Cortical bone dimensions are important determinants of bone strength. Gender differences in cortical bone size caused by greater periosteal expansion in males than in females during the pubertal growth spurt are well established both in humans and in experimental animal models. However, the mechanism by which gender influences cortical bone size is still a matter of investigation. The role of androgens and estrogen in pubertal bone growth has been examined in human disorders as well as animal models, such as gonadectomized or sex steroid receptor knockout mice. Based on the findings that growth hormone (GH) and insulin-like growth factor I (IGF-I) are major regulators of postnatal skeletal growth, we and others have predicted that sex hormones interact with the GH/IGF-I axis to regulate cortical bone size. However, studies conflict as to whether estrogen and androgens impact cortical bone size through the canonical pathway, through GH without IGF-I mediation, through IGF-I without GH stimulation, or independent of GH/IGF-I. We review recent data on the impact of sex steroids and components of the GH/IGF axis on sexual dimorphism in bone size. While the GH/IGF-I axis is a major player in regulating peak bone size, the relative contribution of GH/IGF-dependent mechanisms to sex differences in cortical bone size remains to be established.

Indexed as

Sex CharacteristicsAnimalsBone and BonesBone DevelopmentFemaleGrowth HormoneHumansInsulin-Like Growth Factor IMaleMiceMice, KnockoutModels, BiologicalOrgan SizeSignal TransductionGrowth HormoneInsulin-Like Growth Factor I

Identifiers

PMID21113585
PMCPMC3042806
OpenAlexW2075969984

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.