Evidence map›Paper›PMID 29596063›Full record

ArticleThe Journal of clinical investigation2018

Neuronal hypothalamic regulation of body metabolism and bone density is galanin dependent.

Anna Idelevich, Kazusa Sato, Kenichi Nagano, Glenn Rowe, Francesca Gori, Roland Baron

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-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

22 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Biochemical and Physiological Effects of Galanin in Health and Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  3. Review
  4. Bidirectional Interaction Between the Brain and Bone in Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Anxiety and Depression: What Do We Know of Neuropeptides?Behavioral sciences (Basel, Switzerland) · 2022
    Review
  12. Article
  13. Biological Deciphering of the "Kidney Governing Bones" Theory in Traditional Chinese Medicine.Evidence-based complementary and alternative medicine : eCAM · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. ΔFosB Requires Galanin, but not Leptin, to Increase Bone Mass via the Hypothalamus, but both are needed to increase Energy expenditure.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2019
    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

6 authors at 1 institution in 1 country.

Anna Idelevich
Kazusa Sato
Kenichi Nagano
Glenn Rowe
Francesca Gori
Roland Baron
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

In the brain, the ventral hypothalamus (VHT) regulates energy and bone metabolism. Whether this regulation uses the same or different neuronal circuits is unknown. Alteration of AP1 signaling in the VHT increases energy expenditure, glucose utilization, and bone density, yet the specific neurons responsible for each or all of these phenotypes are not identified. Using neuron-specific, genetically targeted AP1 alterations as a tool in adult mice, we found that agouti-related peptide-expressing (AgRP-expressing) or proopiomelanocortin-expressing (POMC-expressing) neurons, predominantly present in the arcuate nucleus (ARC) within the VHT, stimulate whole-body energy expenditure, glucose utilization, and bone formation and density, although their effects on bone resorption differed. In contrast, AP1 alterations in steroidogenic factor 1-expressing (SF1-expressing) neurons, present in the ventromedial hypothalamus (VMH), increase energy but decrease bone density, suggesting that these effects are independent. Altered AP1 signaling also increased the level of the neuromediator galanin in the hypothalamus. Global galanin deletion (VHT galanin silencing using shRNA) or pharmacological galanin receptor blockade counteracted the observed effects on energy and bone. Thus, AP1 antagonism reveals that AgRP- and POMC-expressing neurons can stimulate body metabolism and increase bone density, with galanin acting as a central downstream effector. The results obtained with SF1-expressing neurons, however, indicate that bone homeostasis is not always dictated by the global energy status, and vice versa.

Indexed as

Bone DensityEnergy MetabolismAnimalsArcuate Nucleus of HypothalamusGalaninGlucoseMiceMice, TransgenicNeuronsPro-OpiomelanocortinGalaningalanin protein, mouseGlucosePro-OpiomelanocortinBone BiologyMetabolismOsteoporosis

Identifiers

PMID29596063
PMCPMC5983337
OpenAlexW2794595575

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.