The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Leptin Inhibits Osteoclast Generation
Open accessAbstract
Originally, leptin was described as a product of adipocytes that acts on the hypothalamus to regulate appetite. However, subsequently, it has been shown that leptin receptors are distributed widely and that leptin has diverse functions, including promotion of hemopoietic and osteoblastic differentiation. It has been recognized for some time that both serum leptin and bone mass are correlated positively to body fat mass and, recently, we have shown a direct positive relationship between serum leptin and bone mass in nonobese women. We now report that leptin inhibits osteoclast generation in cultures of human peripheral blood mononuclear cells (PBMCs) and murine spleen cells incubated on bone in the presence of human macrophage colony-stimulating factor (hM-CSF) and human soluble receptor activator of NF-κB ligand (sRANKL). The half-maximal concentration inhibitory of leptin was approximately 20 nM in the presence of sRANKL at 40 ng/ml but decreased to approximately 2 nM when sRANKL was used at 5 ng/ml. The majority of the inhibitory effect occurred in the first week of the 3-week cultures. Inhibition did not occur when the PBMC cultures were washed vigorously to remove nonadherent cells or when purified CD14+ monocytes were used to generate osteoclasts, indicating an indirect or permissive effect via CD14− PBMC. Leptin increased osteoprotegerin (OPG) messenger RNA (mRNA) and protein expression in PBMC but not in CD14+ cells, suggesting that the inhibitory effect may be mediated by the RANKL/RANK/OPG system. Leptin may act locally to increase bone mass and may contribute to linkage of bone formation and resorption.
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Citations
Cites
Leptin and the regulation of body weight in mammals
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RANK Is the Essential Signaling Receptor for Osteoclast Differentiation Factor in Osteoclastogenesis
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Self-citation
Cited by
Theoleyre, S., Wittrant, Y., Tat, S. K., Fortun, Y., Redini, F., & Heymann, D. (2004) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2004.06.004 · Cited by 663
Leptin in Human Physiology and Pathophysiology
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Relationships between fat and bone
Reid, I. R. (2008) · Osteoporosis International · doi:10.1007/s00198-007-0492-z · Cited by 475
Leptin directly regulates bone cell function in vitro and reduces bone fragility in vivo
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Self-citationLeptin is an effective treatment for hypothalamic amenorrhea
Chou, S. H., Chamberland, J. P., Liu, X., Matarese, G., Gao, C., Stefanakis, R., Brinkoetter, M. T., Gong, H., Arampatzi, K., & Mantzoros, C. S. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1015674108 · Cited by 287
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Bone, Body Weight, and Weight Reduction: What Are the Concerns?
Shapses, S. A., & Riedt, C. S. (2006) · The Journal of Nutrition · doi:10.1093/jn/136.6.1453 · Cited by 247
Effects of Leptin on the Skeleton
Reid, I. R., Baldock, P. A., & Cornish, J. (2018) · Endocrine Reviews · doi:10.1210/er.2017-00226 · Cited by 215
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Leptin in osteoarthritis and rheumatoid arthritis: Player or bystander?
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The Influence of Adipokines on Radiographic Damage in Inflammatory Rheumatic Diseases
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Metadata
- Authors
- Holloway, W. R., Collier, F. M., Aitken, C. J., Myers, D. E., Hodge, J. M., Malakellis, M., Gough, T. J., Collier, G. R., & Prof. Nicholson, G. C.
- Venue
- Journal of Bone and Mineral Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2002-02-01
- Volume
- 17
- Issue
- 2
- Pages
- 200-209
- ISSN
- 0884-0431 (ISSN-L)
- 1523-4681
- OpenAlex
- W2087404413
- Cited by
- 440
- References
- 7
- FWCI
- 8.21
- Type
- journal article
- Language
- en
- Open access
- green
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