Evidence map›Paper›PMID 24532817›Full record

ReviewThe Journal of endocrinology2014

Endocrine regulation of fetal skeletal muscle growth: impact on future metabolic health.

Laura D Brown

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
17.7field-weighted citation impact, top 1% 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

82 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Slow-twitch oxidative myofiber proportions and capillary number per myofiber are reduced in growth-restricted fetal sheep.American journal of physiology. Regulatory, integrative and comparative physiology · 2025
    Article
  7. Article
  8. Tissue-Specific Expression of the PorcineAnimals : an open access journal from MDPI · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Microvascular Skeletal-Muscle Crosstalk in Health and Disease.International journal of molecular sciences · 2023
    Review
  18. The emergence of the stem cell niche.Trends in cell biology · 2023
    Review
  19. Review
  20. Article

22 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

1 author at 1 institution in 1 country.

Laura D BrownDepartment of Pediatrics (Neonatology), Perinatal Research Center, University of Colorado School of Medicine, Anschutz Medical Campus F441, 13243 East 23rd Avenue, Aurora, Colorado 80045, USA.
University of Colorado Denver · US

Funding

UCHSC: Building Interdisciplinary Research Careers in Women's HealthK12HD057022 · NICHD · UNIVERSITY OF COLORADO DENVER · PI REGENSTEINER, JUDITH G., SANTORO, NANETTE F. · 2007 to 2023
$8.5M
NICHD NIH HHS K12 HD057022NICHD NIH HHS K12-HD057022
6 · The paper itself

Abstract

Establishing sufficient skeletal muscle mass is essential for lifelong metabolic health. The intrauterine environment is a major determinant of the muscle mass that is present during the life course of an individual, because muscle fiber number is set at the time of birth. Thus, a compromised intrauterine environment from maternal nutrient restriction or placental insufficiency that restricts muscle fiber number can have permanent effects on the amount of muscle an individual will live with. Reduced muscle mass due to fewer muscle fibers persists even after compensatory or 'catch-up' postnatal growth occurs. Furthermore, muscle hypertrophy can only partially compensate for this limitation in fiber number. Compelling associations link low birth weight and decreased muscle mass to future insulin resistance, which can drive the development of the metabolic syndrome and type 2 diabetes, and the risk of cardiovascular events later in life. There are gaps in knowledge about the origins of reduced muscle growth at the cellular level and how these patterns are set during fetal development. By understanding the nutrient and endocrine regulation of fetal skeletal muscle growth and development, we can direct research efforts toward improving muscle growth early in life to prevent the development of chronic metabolic diseases later in life.

Indexed as

AnimalsEndocrine SystemFemaleFetal DevelopmentFoodHumansIntercellular Signaling Peptides and ProteinsMaternal Nutritional Physiological PhenomenaMuscle, SkeletalPregnancyPrenatal Exposure Delayed EffectsIntercellular Signaling Peptides and Proteinsamino acidsIGF1insulinmuscleneonatalprotein synthesis

Identifiers

PMID24532817
PMCPMC4004098
OpenAlexW2145731761

What Socratic 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 Socratic graph.