New role of bone morphogenetic protein 7 in brown adipogenesis and energy expenditure
Open accessAbstract
Adipose tissue is central to the regulation of energy balance. Two functionally different types of fat are present in mammals: white adipose tissue, the primary site of triglyceride storage, and brown adipose tissue, which is specialized in energy expenditure and can counteract obesity. Factors that specify the developmental fate and function of white and brown adipose tissue remain poorly understood. Here we demonstrate that whereas some members of the family of bone morphogenetic proteins (BMPs) support white adipocyte differentiation, BMP7 singularly promotes differentiation of brown preadipocytes even in the absence of the normally required hormonal induction cocktail. BMP7 activates a full program of brown adipogenesis including induction of early regulators of brown fat fate PRDM16 (PR-domain-containing 16; ref. 4) and PGC-1alpha (peroxisome proliferator-activated receptor-gamma (PPARgamma) coactivator-1alpha; ref. 5), increased expression of the brown-fat-defining marker uncoupling protein 1 (UCP1) and adipogenic transcription factors PPARgamma and CCAAT/enhancer-binding proteins (C/EBPs), and induction of mitochondrial biogenesis via p38 mitogen-activated protein (MAP) kinase-(also known as Mapk14) and PGC-1-dependent pathways. Moreover, BMP7 triggers commitment of mesenchymal progenitor cells to a brown adipocyte lineage, and implantation of these cells into nude mice results in development of adipose tissue containing mostly brown adipocytes. Bmp7 knockout embryos show a marked paucity of brown fat and an almost complete absence of UCP1. Adenoviral-mediated expression of BMP7 in mice results in a significant increase in brown, but not white, fat mass and leads to an increase in energy expenditure and a reduction in weight gain. These data reveal an important role of BMP7 in promoting brown adipocyte differentiation and thermogenesis in vivo and in vitro, and provide a potential new therapeutic approach for the treatment of obesity.
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BMP-7 triggers commitment of mesenchymal progenitor cells to a brown adipocyte lineage and also plays a critical role in embryonic brown fat development, as exemplified by the BMP-7 knockout embryo that shows a marked paucity of brown fat and near complete absence of UCP1.
“Moreover, BMP-7 triggers commitment of mesenchymal progenitor cells to a brown adipocyte lineage and also plays a critical role in embryonic brown fat development, as exemplified by the BMP-7 knockout embryo that shows a marked paucity of brown fat and near complete absence of UCP1 101.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [101]
BMP-2 and 4 promote white fat differentiation, while BMP-7 serves as a potent inductive signal for brown adipogenesis.
“While BMP-2 and 4 promote white fat differentiation, BMP-7 serves as a potent inductive signal for brown adipogenesis 101.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [101]
BMP-7 activates a full program of brown adipogenesis including induction of early regulators of brown fat fate - PRDM16 and PGC-1α, increased expression of adipogenic transcription factors - PPARγ and C/EBPs, mitochondrial biogenesis, and increased expression of UCP1.
“BMP-7 activates a full program of brown adipogenesis including induction of early regulators of brown fat fate - PRDM16 and PGC-1α, increased expression of adipogenic transcription factors - peroxisome proliferator-activated receptor (PPAR)γ and CCAAT/enhancer-binding proteins (C/EBPs), mitochondrial biogenesis, and increased expression of UCP1 (Figure 3).”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [101]
Adenoviral-mediated expression of BMP-7 in mice results in a significant increase in brown, but not white, fat mass and leads to an increase in energy expenditure and reduced weight gain.
“Adenoviral-mediated expression of BMP-7 in mice results in a significant increase in brown, but not white, fat mass and leads to an increase in energy expenditure and reduced weight gain 101.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [101]
When systemically expressed in mice, BMP-7 leads to reduced weight gain.
“When systemically expressed in mice, BMP-7 leads to reduced weight gain 101, suggesting that it may have anti-obesity potential, although more study is needed to determine an optimal therapeutic approach and if there will be any unwanted side effects.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [101]
BMP-7 may have anti-obesity potential.
“When systemically expressed in mice, BMP-7 leads to reduced weight gain 101, suggesting that it may have anti-obesity potential, although more study is needed to determine an optimal therapeutic approach and if there will be any unwanted side effects.”
From Cellular bioenergetics as a target for obesity therapy (2010) · cites this paper as [101]
BMP7 and BMP8B regulate BAT thermogenic function and increase EE.
“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 Tseng et al., 2008
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Goody, D., & Pfeifer, A. (2019) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2018.05.003 · Cited by 54 · see citing works
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Post-exercise changes in myostatin and actRIIB expression in obese insulin-resistant rats
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- Authors
- Tseng, Y.-H., Kokkotou, E., Schulz, T. J., Huang, T. L., Winnay, J. N., Taniguchi, C. M., Tran, T. T., Suzuki, R., Espinoza, D. O., Yamamoto, Y., Ahrens, M. J., Dudley, A. T., Norris, A. W., Kulkarni, R. N., & Kahn, C. R.
- Affiliations
- Joslin Diabetes Center (US)
- Beth Israel Deaconess Medical Center (US)
- Harvard University (US)
- Northwestern University (US)
- University of Iowa (US)
- Corresponding author
- Tseng, Yu-Hua
- ORCID
- Venue
- Nature
- Published
- 2008-08-21
- Volume
- 454
- Issue
- 7207
- Pages
- 1000-1004
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC2745972
- OpenAlex
- W1981525131
- Cited by
- 1,099
- References
- 34
- Citations by year
- 2026: 33 · 2025: 28 · 2024: 43 · 2023: 47 · 2022: 52 · 2021: 53 · 2020: 70 · 2019: 68 · 2018: 66 · 2017: 76 · 2016: 76 · 2015: 92 · 2014: 80 · 2013: 81 · 2012: 68
- FWCI
- 37.24
- Type
- journal article
- Language
- en
- Update notices
- erratum (2009-05-07)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK077097, R01 DK-67536, R21DK070722, P30DK046200, K08DK064906, P30 DK-46200, R01DK060837, K08 DK64906, R01DK067536, P30DK040561)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- bone morphogenetic protein-7, BMP-7, brown adipogenesis, brown adipose tissue, energy expenditure, energy homeostasis, PRDM16, PGC-1α, mitochondrial biogenesis, PPARγ, C/EBP, UCP1, p38 MAPK, mesenchymal progenitor cells, obesity, adipose tissue differentiation
- MeSH terms
- Animals, Adipose Tissue, Brown, Cell Line, Energy Metabolism, Male, Mice, Inbred C57BL, Mice, Nude, Mitochondria, Transforming Growth Factor beta, Bone Morphogenetic Proteins, Thermogenesis, 3T3-L1 Cells, p38 Mitogen-Activated Protein Kinases, Adipogenesis, Mice, Adipose Tissue, White, Bone Morphogenetic Protein 7, Mesenchymal Stem Cells
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