Evidence map›Paper›PMID 28149508›Full record

ReviewBoneKEy reports2016

Protein/amino-acid modulation of bone cell function.

Robert MacDonell, Mark W Hamrick, Carlos M Isales

Open access · greenAbstract readReview
In one paragraph

Review in BoneKEy reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Discovery of potential biomarkers for osteoporosis using LC-MS/MS metabolomic methods.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2019
    Article
  18. Article
  19. The positive association of total protein intake with femoral neck strength (KNHANES IV).Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2018
    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

3 authors at 1 institution in 1 country.

Robert MacDonellInstitute for Regenerative and Reparative Medicine, Medical College of Georgia, Augusta University , Augusta, GA, USA.
Mark W HamrickInstitute for Regenerative and Reparative Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA; Departments of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, GA, USA; Departments of Orthopaedic Surgery, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Carlos M IsalesInstitute for Regenerative and Reparative Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA; Departments of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, GA, USA; Departments of Orthopaedic Surgery, Medical College of Georgia, Augusta University, Augusta, GA, USA; Departments of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA; Departments of Medicine, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Augusta University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nutrients (protein, carbohydrates and fats) have traditionally been thought of as fuels simply providing the energy for cellular metabolic activity. According to the classic view, if nutrients are available, then anabolic pathways are activated, and if nutrients are not available, catabolic pathways are activated. However, it is becoming increasingly clear that nutrient effects on bone cells (stem cells, osteoblasts and osteoclasts) are complex, some nutrients promote bone formation, whereas others interfere with bone formation or actually promote bone break down. At an organ level, nutrient intake can suppress bone breakdown and modulate the activity of the calcium/vitamin D/parathyroid hormone axis. At a cellular level, nutrient intake can impact cellular energetics either through a direct mechanism (binding or uptake of the nutrient into the cell) or indirect (by elevating nutrient-related hormones such as insulin, insulin-like growth factor 1 or incretin hormones). It is also becoming clear that within a nutrient class (for example, protein), individual components (that is, amino acids) can have markedly different effects on cell function and impact bone formation. The focus of this review will be on one nutrient class in particular, dietary protein. As the prevalence of inadequate dietary protein intake increases with age, these findings may have translational implications as to the optimal dietary protein content in the setting of age-associated bone loss.

Identifiers

PMID28149508
PMCPMC5238414
OpenAlexW2488001853

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.