Regulation of Osteoblast Metabolism by Wnt Signaling
Wnt/β-catenin signaling plays a critical role in the achievement of peak bone mass, affecting the commitment of mesenchymal progenitors to the osteoblast lineage and the anabolic capacity of osteoblasts depositing bone matrix. Recent studies suggest that this evolutionarily-conserved, developmental...
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| Format: | Article |
| Language: | English |
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Korean Endocrine Society
2018-08-01
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| Series: | Endocrinology and Metabolism |
| Subjects: | |
| Online Access: | https://e-enm.org/Synapse/Data/PDFData/2008ENM/enm-33-318.pdf |
| _version_ | 1811272210333040640 |
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| author | Megan C. Moorer Ryan C. Riddle |
| author_facet | Megan C. Moorer Ryan C. Riddle |
| author_sort | Megan C. Moorer |
| collection | DOAJ |
| description | Wnt/β-catenin signaling plays a critical role in the achievement of peak bone mass, affecting the commitment of mesenchymal progenitors to the osteoblast lineage and the anabolic capacity of osteoblasts depositing bone matrix. Recent studies suggest that this evolutionarily-conserved, developmental pathway exerts its anabolic effects in part by coordinating osteoblast activity with intermediary metabolism. These findings are compatible with the cloning of the gene encoding the low-density lipoprotein related receptor-5 (LRP5) Wnt co-receptor from a diabetes-susceptibility locus and the now well-established linkage between Wnt signaling and metabolism. In this article, we provide an overview of the role of Wnt signaling in whole-body metabolism and review the literature regarding the impact of Wnt signaling on the osteoblast's utilization of three different energy sources: fatty acids, glucose, and glutamine. Special attention is devoted to the net effect of nutrient utilization and the mode of regulation by Wnt signaling. Mechanistic studies indicate that the utilization of each substrate is governed by a unique mechanism of control with β-catenin-dependent signaling regulating fatty acid β-oxidation, while glucose and glutamine utilization are β-catenin-independent and downstream of mammalian target of rapamycin complex 2 (mTORC2) and mammalian target of rapamycin complex 1 (mTORC1) activation, respectively. The emergence of these data has provided a new context for the mechanisms by which Wnt signaling influences bone development. |
| first_indexed | 2024-04-12T22:36:06Z |
| format | Article |
| id | doaj.art-636134efb9ac445c82cc702ba4a264f5 |
| institution | Directory Open Access Journal |
| issn | 2093-596X 2093-5978 |
| language | English |
| last_indexed | 2024-04-12T22:36:06Z |
| publishDate | 2018-08-01 |
| publisher | Korean Endocrine Society |
| record_format | Article |
| series | Endocrinology and Metabolism |
| spelling | doaj.art-636134efb9ac445c82cc702ba4a264f52022-12-22T03:13:51ZengKorean Endocrine SocietyEndocrinology and Metabolism2093-596X2093-59782018-08-0133331833010.3803/EnM.2018.33.3.318Regulation of Osteoblast Metabolism by Wnt SignalingMegan C. Moorer0Ryan C. Riddle1Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, .USADepartment of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, .USAWnt/β-catenin signaling plays a critical role in the achievement of peak bone mass, affecting the commitment of mesenchymal progenitors to the osteoblast lineage and the anabolic capacity of osteoblasts depositing bone matrix. Recent studies suggest that this evolutionarily-conserved, developmental pathway exerts its anabolic effects in part by coordinating osteoblast activity with intermediary metabolism. These findings are compatible with the cloning of the gene encoding the low-density lipoprotein related receptor-5 (LRP5) Wnt co-receptor from a diabetes-susceptibility locus and the now well-established linkage between Wnt signaling and metabolism. In this article, we provide an overview of the role of Wnt signaling in whole-body metabolism and review the literature regarding the impact of Wnt signaling on the osteoblast's utilization of three different energy sources: fatty acids, glucose, and glutamine. Special attention is devoted to the net effect of nutrient utilization and the mode of regulation by Wnt signaling. Mechanistic studies indicate that the utilization of each substrate is governed by a unique mechanism of control with β-catenin-dependent signaling regulating fatty acid β-oxidation, while glucose and glutamine utilization are β-catenin-independent and downstream of mammalian target of rapamycin complex 2 (mTORC2) and mammalian target of rapamycin complex 1 (mTORC1) activation, respectively. The emergence of these data has provided a new context for the mechanisms by which Wnt signaling influences bone development.https://e-enm.org/Synapse/Data/PDFData/2008ENM/enm-33-318.pdfWnt signalingBeta cateninOsteoblastsIntermediary metabolism |
| spellingShingle | Megan C. Moorer Ryan C. Riddle Regulation of Osteoblast Metabolism by Wnt Signaling Endocrinology and Metabolism Wnt signaling Beta catenin Osteoblasts Intermediary metabolism |
| title | Regulation of Osteoblast Metabolism by Wnt Signaling |
| title_full | Regulation of Osteoblast Metabolism by Wnt Signaling |
| title_fullStr | Regulation of Osteoblast Metabolism by Wnt Signaling |
| title_full_unstemmed | Regulation of Osteoblast Metabolism by Wnt Signaling |
| title_short | Regulation of Osteoblast Metabolism by Wnt Signaling |
| title_sort | regulation of osteoblast metabolism by wnt signaling |
| topic | Wnt signaling Beta catenin Osteoblasts Intermediary metabolism |
| url | https://e-enm.org/Synapse/Data/PDFData/2008ENM/enm-33-318.pdf |
| work_keys_str_mv | AT megancmoorer regulationofosteoblastmetabolismbywntsignaling AT ryancriddle regulationofosteoblastmetabolismbywntsignaling |