The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Leptin and the sympathetic connection of fat to bone
Open accessAbstract
Loss of body weight is associated with bone loss, and body weight gain is associated with increased bone formation. The molecular mechanisms linking body weight, body composition, and bone density are now better understood. Lean mass is likely to have a significant, local effect on bone modeling and remodeling through mechanotransduction pathways. In contrast to the local regulation of bone formation and resorption by muscle-derived stimuli, peripheral body fat appears to influence bone mass via secretion of systemic, endocrine factors that link body weight to bone density even in non-weight bearing regions (e.g., the forearm). The cytokine-like hormone leptin, which is secreted by fat cells, is an important candidate molecule linking changes in body composition with bone formation and bone resorption. Increases in body fat increase leptin levels and stimulate periosteal bone formation through its direct anabolic effects on osteoblasts, and through central (CNS) effects including the stimulation of the GH-IGF-1 axis and suppression of neuropeptide Y, a powerful inhibitor of bone formation. Stimulation of beta2-adrenergic receptors through central (hypothalamic) leptin receptors does, however, increase remodeling of trabecular bone, resulting in a lower cancellous bone volume that may be better adapted to a concomitantly larger cortical bone compartment. These findings suggest that body weight and body fat can regulate bone mass and structure through molecular pathways that are independent of load-bearing. Furthermore, pharmacological manipulation of the signaling pathways activated by leptin may have significant potential for the treatment and prevention of bone loss.
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Cites
Obesity and Metabolic Syndrome in Circadian Clock Mutant Mice
Turek, F. W., Joshu, C., Kohsaka, A., Lin, E., Ivanova, G., McDearmon, E., Laposky, A., Losee-Olson, S., Easton, A., Jensen, D. R., et al. (2005) · Science · doi:10.1126/science.1108750 · Cited by 2,485
Leptin Inhibits Bone Formation through a Hypothalamic Relay
Ducy, P., Amling, M., Takeda, S., Priemel, M., Schilling, A. F., Beil, F. T., Shen, J., Vinson, C., Rueger, J. M., & Karsenty, G. (2000) · Cell · doi:10.1016/s0092-8674(00)81558-5 · Cited by 2,077
Leptin Regulates Bone Formation via the Sympathetic Nervous System
Takeda, S., Elefteriou, F., Levasseur, R., Liu, X., Zhao, L., Parker, K. L., Armstrong, D., Ducy, P., & Karsenty, G. (2002) · Cell · doi:10.1016/s0092-8674(02)01049-8 · Cited by 1,735
Leptin regulation of bone resorption by the sympathetic nervous system and CART
Elefteriou, F., Ahn, J. D., Takeda, S., Starbuck, M., Yang, X., Liu, X., Kondo, H., Richards, W. G., Bannon, T. W., Noda, M., et al. (2005) · Nature · doi:10.1038/nature03398 · Cited by 1,311 · cited 5×
“These effects appear to be primarily, if not uniquely, mediated by beta2 adrenergic receptors expressed in osteoblasts [59], as several investigators, including ourselves, failed to detect significant expression of beta1 and beta3 adrenergic receptor genes (ADRB1, ADRB3) in primary osteoblastic cells from mouse calvar…”
InfluentialRecombinant human leptin in women with hypothalamic amenorrhea
Welt, C. K., Chan, J. L., Bullen, J., Murphy, R., Smith, P., DePaoli, A. M., Karalis, A., & Mantzoros, C. S. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa040388 · Cited by 908
Unraveling the central nervous system pathways underlying responses to leptin
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β-Blocker Use, BMD, and Fractures in the Study of Osteoporotic Fractures
Reid, I. R., Gamble, G. D., Grey, A. B., Black, D. M., Ensrud, K. E., Browner, W. S., & Bauer, D. C. (2005) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.041202 · Cited by 156
Martin, A., David, V., Malaval, L., Lafage-Proust, M.-H., Vico, L., & Thomas, T. (2007) · Endocrinology · doi:10.1210/en.2006-1541 · Cited by 111
Cited by
Mechanisms of diabetes mellitus-induced bone fragility
On behalf of the IOF Bone and Diabetes Working Group, Napoli, N., Chandran, M., Pierroz, D. D., Abrahamsen, B., Schwartz, A. V., & Ferrari, S. L. (2017) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2016.153 · Cited by 1,107
Self-citationAutonomic Nervous System and Immune System Interactions
Kenney, M. J., & Ganta, C. K. (2014) · Comprehensive Physiology · doi:10.1002/cphy.c130051 · Cited by 381
Hamrick, M. W., Ding, K.-H., Ponnala, S., Ferrari, S. L., & Isales, C. M. (2008) · Journal of Bone and Mineral Research · doi:10.1359/jbmr.080213 · Cited by 143
Self-citationRole of the Cytokine-like Hormone Leptin in Muscle-bone Crosstalk with Aging
Hamrick, M. W. (2017) · Journal of Bone Metabolism · doi:10.11005/jbm.2017.24.1.1 · Cited by 77
Self-citationIwaniec, U. T., Boghossian, S., Trevisiol, C. H., Wronski, T. J., Turner, R. T., & Kalra, S. P. (2011) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.365 · Cited by 24
Metadata
- Authors
- Hamrick, M. W., & Ferrari, S. L.
- Venue
- Osteoporosis International
- Published
- 2007-10-09
- Volume
- 19
- Issue
- 7
- Pages
- 905-912
- ISSN
- 0937-941X (ISSN-L)
- 1433-2965
- OpenAlex
- W2133837081
- Cited by
- 221
- References
- 8
- FWCI
- 6.59
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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