Evidence map›Paper›PMID 22534195›Full record

ReviewBiochimie2012

Understanding leptin-dependent regulation of skeletal homeostasis.

Katherine J Motyl, Clifford J Rosen

Abstract readReview
In one paragraph

Review in Biochimie, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.8field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 104 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Editorial: Bone-organ axis: an expanding universe.Frontiers in endocrinology · 2025
    Article
  6. Review
  7. Review
  8. Review
  9. Obesity, diabetes and risk of bone fragility: How BMAT behavior is affected by metabolic disturbances and its influence on bone health.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. The Role of Irisin in Exercise-Mediated Bone Health.Frontiers in cell and developmental biology · 2021
    Review
  17. Article
  18. Review
  19. Article
  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.

Katherine J MotylMaine Medical Center Research Institute, 81 Research Drive, Scarborough, ME, USA. motylk@mmc.org
Clifford J Rosen
Maine Medical Center · US

Funding

Interdisciplinary Study of Marrow Adiposity, Mineral Metabolism & Energy BalanceR24DK092759 · NIDDK · MAINEHEALTH · PI HOROWITZ, MARK C, MACDOUGALD, ORMOND A · 2011 to 2019
$13.0M
Misty: a model for central regulation of bone remodelingR01AG040217 · NIA · MAINEHEALTH · PI ROSEN, CLIFFORD JAMES · 2011 to 2015
$1.7M
Mechanisms of Bone Loss from Administration of the Second-Generation AntipsychotiF32AR061932 · NIAMS · MAINEHEALTH · PI MOTYL, KATHERINE JEAN · 2011 to 2013
$157k
NIAMS NIH HHS AR061932NIAMS NIH HHS F32 AR061932NIA NIH HHS AG040219NIA NIH HHS R01 AG040217NIDDK NIH HHS DK092759NIDDK NIH HHS R24 DK092759
6 · The paper itself

Abstract

Despite growing evidence for adipose tissue regulation of bone mass, the role of the adipokine leptin in bone remodeling remains controversial. The majority of in vitro studies suggest leptin enhances osteoblastic proliferation and differentiation while inhibiting adipogenic differentiation from marrow stromal cells. Alternatively, some evidence demonstrates either no effect or a pro-apoptotic action of leptin on stromal cells. Similarly, in vivo work has demonstrated both positive and negative effects of leptin on bone mass. Most of the literature supports the idea that leptin suppresses bone mass by acting in the brainstem to reduce serotonin-dependent sympathetic signaling from the ventromedial hypothalamus to bone. However, other studies have found partly or entirely contrasting actions of leptin. Recently one study found a significant effect of surgery alone with intracerebroventricular administration of leptin, a technique crucial for understanding centrally-mediated leptin regulation of bone. Thus, two mainstream hypotheses for the role of leptin on bone emerge: 1) direct regulation through increased osteoblast proliferation and differentiation and 2) indirect suppression of bone formation through a hypothalamic relay. At the present time, it remains unclear whether these effects are relevant in only extreme circumstances (i.e. models with complete deficiency) or play an important homeostatic role in the regulation of peak bone acquisition and skeletal remodeling. Ultimately, determining the actions of leptin on the skeleton will be critical for understanding how the obesity epidemic may be impacting the prevalence of osteoporosis.

Indexed as

HomeostasisAnimalsBone and BonesDrug ResistanceHumansLeptinReceptors, LeptinLeptinReceptors, Leptin

Identifiers

PMID22534195
PMCPMC3512082
OpenAlexW2057357986

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.