Cited by 1,735Bone Metabolism and DiseasesBone health and osteoporosis researchRegulation of Appetite and Obesity

The DOI matches its Crossref record; 51 of the 54 references it cites were found in a registry or an index.

Leptin Regulates Bone Formation via the Sympathetic Nervous System

Open access

Abstract

We previously showed that leptin inhibits bone formation by an undefined mechanism. Here, we show that hypothalamic leptin-dependent antiosteogenic and anorexigenic networks differ, and that the peripheral mediators of leptin antiosteogenic function appear to be neuronal. Neuropeptides mediating leptin anorexigenic function do not affect bone formation. Leptin deficiency results in low sympathetic tone, and genetic or pharmacological ablation of adrenergic signaling leads to a leptin-resistant high bone mass. beta-adrenergic receptors on osteoblasts regulate their proliferation, and a beta-adrenergic agonist decreases bone mass in leptin-deficient and wild-type mice while a beta-adrenergic antagonist increases bone mass in wild-type and ovariectomized mice. None of these manipulations affects body weight. This study demonstrates a leptin-dependent neuronal regulation of bone formation with potential therapeutic implications for osteoporosis.

Overview

Integrity signals

Registry

Crossref · 10.1016/s0092-8674(02)01049-8

Cites

51 of 51 references verified0 citation errors · 0 not checkable

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Claims the paper makes

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Claims other papers make about this one

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  • Leptin deficiency lowers sympathetic tone, leading to higher bone mass, while β-adrenergic blockade or leptin replacement during disuse mitigates bone loss by boosting osteoblast activity, curbing osteoclast function, and maintaining leptin levels to preserve bone density and formation rates.

    “leptin deficiency lowers sympathetic tone, leading to higher bone mass, while β-adrenergic blockade or leptin replacement during disuse mitigates bone loss by boosting osteoblast activity, curbing osteoclast function, and maintaining leptin levels to preserve bone density and formation rates [80,81]”

Citations

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3 of the 54 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. Tremollieres, 1993, Vertebral postmenopausal bone loss is reduced in overweight women, J. Clin. Endocrinol. Metab., 77, 683

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Metadata

Authors
Takeda, S., Elefteriou, F., Levasseur, R., Liu, X., Zhao, L., Parker, K. L., Armstrong, D., Ducy, P., & Karsenty, G.
Affiliations
  • The University of Texas Southwestern Medical Center (US)
  • Baylor College of Medicine (US)
Venue
Cell
Publisher
Elsevier BV
Published
2002-11
Volume
111
Issue
3
Pages
305-317
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2147510409
Cited by
1,735
References
54
Citations by year
2026: 50 · 2025: 58 · 2024: 61 · 2023: 49 · 2022: 55 · 2021: 57 · 2020: 69 · 2019: 70 · 2018: 66 · 2017: 68 · 2016: 66 · 2015: 81 · 2014: 86 · 2013: 71 · 2012: 105
FWCI
23.47
Type
journal article
Language
en
Open access
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK-54480, R01DK058883, R01DK054480, DK58883)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD24054)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
  • Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Keywords
leptin, bone formation, sympathetic nervous system, beta-adrenergic receptors, osteoblast proliferation, leptin resistance, leptin deficiency, hypothalamic neurons, osteoporosis, bone mass, ovariectomy
MeSH terms
Adrenergic beta-Antagonists, Animals, Cells, Cultured, Hypothalamus, Mice, Inbred C57BL, Neuropeptides, Obesity, Oligopeptides, Osteoblasts, Osteogenesis, Pyrrolidonecarboxylic Acid, Receptors, Adrenergic, beta, Sympathetic Nervous System, Receptors, Corticotropin, Leptin, Receptor, Melanocortin, Type 4, Mice, Receptors, Leptin

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