Substantial progress has been made in defining genes and proteins involved in development, maintenance and regeneration of teeth and bones. This knowledge has improved strategies for diagnosing and treating mineralized tissue diseases. Existing data provide credence for these genes/proteins having roles beyond those attributed to mineralized tissues. For example, they may affect systemic metabolic activity and glucose tolerance. One example is fibroblast growth factor 23 (Fgf23), a hormone secreted by osteocytes, suppressing phosphate reabsorption into the blood stream and vitamin D synthesis in the kidney. Many other bone associated proteins, perhaps acting as endocrine factors, are reported to act at distant sites to alter metabolic activity. However, there remains substantial uncertainty as to whether bone itself functioning as an endocrine organ and/or factors secreted by bone could modulate metabolic activity. Such information should be of value toward informing clinical strategies to treat mineralized tissue and metabolic disorders.
For this Research Topic, we welcome manuscripts that highlight the importance of, and expand our knowledge of the interconnections between bone and systemic metabolic activity. Some examples of questions to consider are provided here, and we are open to other related questions.
1. Do hormones that regulate mineralized tissues affect systemic metabolic activity, and contribute to metabolic syndrome when modulation is disrupted?
2. What are the known and postulated functions of genes/proteins identified with bones/teeth in modulating energy metabolism?
3. What factors and molecular mechanisms, known and suggested, control mesodermal pluripotent cells differentiation along the osteogenic vs adipogenic pathway in health and disease states across the life span.
4. What are the roles of macrophages in controlling energy metabolism?
5. Is there evidence that the skeleton acts as an endocrine organ?
6. Is there a direct link between diabetes and osteoporosis?
7. Do the effects of diabetes on bone homeostasis, i.e., alterations in gene/proteins modulating bone homeostasis, affect glucose metabolism and/or other metabolic pathways?
8. What evidence supports a role for brain (neuropeptides) and other organ interactions with bone controlling bone homeostasis, to include networks modulating energy metabolism?
We welcome contributions in the form of original research, review, mini review, case report, hypothesis and theory, perspective, and experimental studies that cover, but are not limited to, the following themes:
1. New strategies for confirming, proving, and identifying genes/proteins secreted by mineralized tissue’s role (s) in modulating energy metabolism.
2. Effect of therapies for treating metabolic syndrome on mineralized tissue homeostasis.
3. Autocrine/paracrine signaling pathways modulating osteogenesis-adipogenesis interactions.
4. Methods and results using animal models, organs, tissues, cells to investigate links between metabolism and mineralized tissue homeostasis, both direct and indirect effects.
5. Effect of nutrition, diet, and environment on modulating mineral tissue homeostasis and resulting effects on metabolism.
6. Interactions between hormones, mineralized tissues and other tissues influencing metabolism.
7. The role of mineralized tissues in health and disease, in affecting metabolic activities throughout the body, across the life span.
Substantial progress has been made in defining genes and proteins involved in development, maintenance and regeneration of teeth and bones. This knowledge has improved strategies for diagnosing and treating mineralized tissue diseases. Existing data provide credence for these genes/proteins having roles beyond those attributed to mineralized tissues. For example, they may affect systemic metabolic activity and glucose tolerance. One example is fibroblast growth factor 23 (Fgf23), a hormone secreted by osteocytes, suppressing phosphate reabsorption into the blood stream and vitamin D synthesis in the kidney. Many other bone associated proteins, perhaps acting as endocrine factors, are reported to act at distant sites to alter metabolic activity. However, there remains substantial uncertainty as to whether bone itself functioning as an endocrine organ and/or factors secreted by bone could modulate metabolic activity. Such information should be of value toward informing clinical strategies to treat mineralized tissue and metabolic disorders.
For this Research Topic, we welcome manuscripts that highlight the importance of, and expand our knowledge of the interconnections between bone and systemic metabolic activity. Some examples of questions to consider are provided here, and we are open to other related questions.
1. Do hormones that regulate mineralized tissues affect systemic metabolic activity, and contribute to metabolic syndrome when modulation is disrupted?
2. What are the known and postulated functions of genes/proteins identified with bones/teeth in modulating energy metabolism?
3. What factors and molecular mechanisms, known and suggested, control mesodermal pluripotent cells differentiation along the osteogenic vs adipogenic pathway in health and disease states across the life span.
4. What are the roles of macrophages in controlling energy metabolism?
5. Is there evidence that the skeleton acts as an endocrine organ?
6. Is there a direct link between diabetes and osteoporosis?
7. Do the effects of diabetes on bone homeostasis, i.e., alterations in gene/proteins modulating bone homeostasis, affect glucose metabolism and/or other metabolic pathways?
8. What evidence supports a role for brain (neuropeptides) and other organ interactions with bone controlling bone homeostasis, to include networks modulating energy metabolism?
We welcome contributions in the form of original research, review, mini review, case report, hypothesis and theory, perspective, and experimental studies that cover, but are not limited to, the following themes:
1. New strategies for confirming, proving, and identifying genes/proteins secreted by mineralized tissue’s role (s) in modulating energy metabolism.
2. Effect of therapies for treating metabolic syndrome on mineralized tissue homeostasis.
3. Autocrine/paracrine signaling pathways modulating osteogenesis-adipogenesis interactions.
4. Methods and results using animal models, organs, tissues, cells to investigate links between metabolism and mineralized tissue homeostasis, both direct and indirect effects.
5. Effect of nutrition, diet, and environment on modulating mineral tissue homeostasis and resulting effects on metabolism.
6. Interactions between hormones, mineralized tissues and other tissues influencing metabolism.
7. The role of mineralized tissues in health and disease, in affecting metabolic activities throughout the body, across the life span.