Evidence map›Paper›PMID 29777919›Full record

ReviewBone2018

Brain to bone: What is the contribution of the brain to skeletal homeostasis?

Anna Idelevich, Roland Baron

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 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

42 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Brain-Bone Axis in Physiological and Pathological Conditions.International journal of molecular sciences · 2025
    Review
  8. Bidirectional Interaction Between the Brain and Bone in Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  9. Review
  10. Article
  11. Relationship of Chronic Stress and Hypertension with Bone Resorption.Journal of functional morphology and kinesiology · 2025
    Review
  12. Review
  13. Article
  14. Connecting the dots: sex, depression, and musculoskeletal health.The Journal of clinical investigation · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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 1 institution in 1 country.

Anna IdelevichDepartment of Medicine, Harvard Medical School and Endocrine Unit MGH, Division of Bone and Mineral Metabolism, Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA.
Roland BaronDepartment of Medicine, Harvard Medical School and Endocrine Unit MGH, Division of Bone and Mineral Metabolism, Department of Oral Medicine, Infection and Immunity, Harvard School of Dental Medicine, Boston, MA, USA. Electronic address: Roland_Baron@hms.harvard.edu.
Harvard University · US

Funding

AP1-dependent regulation of bone mass and energy expenditure in the hypothalamusR01AG040222 · NIA · HARVARD MEDICAL SCHOOL · PI BARON, ROLAND E · 2011 to 2015
$1.9M
NIA NIH HHS R01 AG040222
6 · The paper itself

Abstract

The brain, which governs most, if not all, physiological functions in the body, from the complexities of cognition, learning and memory, to the regulation of basal body temperature, heart rate and breathing, has long been known to affect skeletal health. In particular, the hypothalamus - located at the base of the brain in close proximity to the medial eminence, where the blood-brain-barrier is not as tight as in other regions of the brain but rather "leaky", due to fenestrated capillaries - is exposed to a variety of circulating body cues, such as nutrients (glucose, fatty acids, amino acids), and hormones (insulin, glucagon, leptin, adiponectin) [1-3].Information collected from the body via these peripheral cues is integrated by hypothalamic sensing neurons and glial cells [4-7], which express receptors for these nutrients and hormones, transforming these cues into physiological outputs. Interestingly, many of the same molecules, including leptin, adiponectin and insulin, regulate both energy and skeletal homeostasis. Moreover, they act on a common set of hypothalamic nuclei and their residing neurons, activating endocrine and neuronal systems, which ultimately fine-tune the body to new physiological states. This review will focus exclusively on the brain-to-bone pathway, highlighting the most important anatomical sites within the brain, which are known to affect bone, but not covering the input pathways and molecules informing the brain of the energy and bone metabolic status, covered elsewhere [8-10]. The discussion in each section will present side by side the metabolic and bone-related functions of hypothalamic nuclei, in an attempt to answer some of the long-standing questions of whether energy is affected by bone remodeling and homeostasis and vice versa.

Indexed as

AnimalsBone and BonesBone RemodelingEnergy MetabolismHomeostasisHumansHypothalamusBoneEnergy metabolismHypothalamusPituitary

Identifiers

PMID29777919
PMCPMC6110971
OpenAlexW2803293375

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.