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Bone morphogenetic protein 7 (BMP7) reverses obesity and regulates appetite through a central mTOR pathway
Open accessAbstract
Body weight is regulated by coordinating energy intake and energy expenditure. Transforming growth factor β (TGFβ)/bone morphogenetic protein (BMP) signaling has been shown to regulate energy balance in lower organisms, but whether a similar pathway exists in mammals is unknown. We have previously demonstrated that BMP7 can regulate brown adipogenesis and energy expenditure. In the current study, we have uncovered a novel role for BMP7 in appetite regulation. Systemic treatment of diet‐induced obese mice with BMP7 resulted in increased energy expenditure and decreased food intake, leading to a significant reduction in body weight and improvement of metabolic syndrome. Similar degrees of weight loss with reduced appetite were also observed in BMP7‐treated ob/ob mice, suggesting a leptin‐independent mechanism utilized by BMP7. Intracerebroventricular administration of BMP7 to mice led to an acute decrease in food intake, which was mediated, at least in part, by a central rapamycin‐sensitive mTOR‐p70S6 kinase pathway. Together, these results underscore the importance of BMP7 in regulating both food intake and energy expenditure, and suggest new therapeutic approaches for obesity and its comorbidities.— Townsend, K. L., Suzuki, R., Huang, T. L., Jing, E., Schulz, T. J., Lee, K., Taniguchi, C. M., Espinoza, D. O., McDougall, L. E., Zhang, H., He, T.‐C., Kokkotou, E., Tseng, Y.‐H. Bone morphogenetic protein 7 (BMP7) reverses obesity and regulates appetite through a central mTOR pathway. FASEB J. 26, 2187‐2196 (2012). www.fasebj.org
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“Thus, BMP7 and BMP8B were demonstrated to regulate BAT thermogenic function and increase EE (Tseng et al., 2008, Townsend et al., 2012, Townsend et al., 2013, Whittle et al., 2012).”
From A Functional Link between AMPK and Orexin Mediates the Effect of BMP8B on Energy Balance (2016) · cites this paper as Townsend et al., 2012
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Metadata
- Authors
- Townsend, K. L., Suzuki, R., Huang, T. L., Jing, E., Schulz, T. J., Lee, K., Taniguchi, C. M., Espinoza, D. O., McDougall, L. E., Zhang, H., He, T., Kokkotou, E., & Tseng, Y.
- Affiliations
- Joslin Diabetes Center (US)
- University of Chicago (US)
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Kokkotou, Efi
- Tseng, Yu‐Hua
- ORCID
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2012-02-13
- Volume
- 26
- Issue
- 5
- Pages
- 2187-2196
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- PMC
- PMC3336788
- OpenAlex
- W2115947337
- Cited by
- 105
- References
- 61
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 3 · 2023: 6 · 2022: 8 · 2021: 9 · 2020: 5 · 2019: 9 · 2018: 8 · 2017: 6 · 2016: 9 · 2015: 8 · 2014: 13 · 2013: 13 · 2012: 2
- FWCI
- 5.14
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The FASEB Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (NIH R01 DK077097, UL1 RR 025758‐01, R01 DK080058, T32‐DK007260‐33, F32‐DK091996)
- Harvard Stem Cell Institute
- National Institute of Diabetes and Digestive and Kidney Diseases (P30‐DK036836)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- bone morphogenetic protein-7, obesity, appetite regulation, dietary intake, energy expenditure, mTOR signaling, p70 S6 kinase, TGF-β/BMP signaling, metabolic syndrome, brown adipogenesis, ob/ob mice, central nervous system
- MeSH terms
- Animals, Appetite, Cells, Cultured, Injections, Intraventricular, Obesity, In Situ Hybridization, Reverse Transcriptase Polymerase Chain Reaction, Mice, Bone Morphogenetic Protein 7, TOR Serine-Threonine Kinases
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