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Involvement of bone in systemic endocrine regulation.

I Zofkova1

  • 1Institute of Endocrinology, Prague 1, Czech Republic. izofkova@upcmail.cz.

Physiological Research
|July 26, 2018
PubMed
Summary

Bone is not only a structural tissue but also an endocrine organ. Osteocytes and osteoblasts produce hormones that influence phosphate and energy balance. These hormones affect the kidney, parathyroid glands, and other organs. Osteocalcin modulates functions in the pancreas, muscle, brain, and testes. This review highlights the broader endocrine role of bone and its impact on systemic health.

Keywords:
bone endocrinologyphosphate regulationosteoblast functionFGF23 role

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Area of Science:

  • Endocrinology and metabolic regulation
  • Skeletal biology and bone remodeling
  • Renal physiology and mineral homeostasis

Background:

The role of bone in endocrine regulation is an emerging area of research. Prior studies have established bone as a target for systemic hormones. However, recent evidence suggests that bone itself acts as an endocrine organ. This shift in understanding highlights the need to explore how bone-derived hormones influence other systems. Bone cells, particularly osteocytes, are now recognized as key players in this process. These cells respond to mechanical and hormonal signals. They regulate bone remodeling and also produce signaling molecules. The connection between bone and phosphate metabolism is well-documented. However, the broader endocrine functions of bone remain less understood.

Purpose Of The Study:

This review aims to examine how bone hormones interact with phosphate and energy homeostasis. The focus is on the hormonal network involving osteocytes and osteoblasts. The study explores the role of these cells in regulating phosphate metabolism. It also investigates their influence on energy balance and reproduction. The authors seek to clarify the mechanisms through which bone hormones act. They highlight the role of vitamin D derivatives and phosphatonins. The goal is to synthesize current knowledge on these interactions. This work addresses a gap in understanding the systemic effects of bone-derived hormones.

Main Methods:

The authors conducted a literature review focusing on bone endocrinology. They examined studies on osteocytes and osteoblasts as endocrine cells. The review included research on bone-derived hormones like sclerostin and FGF23. They analyzed the interaction of these hormones with kidney and parathyroid functions. The study also looked at how osteocalcin affects other tissues. The authors synthesized findings on phosphate and energy regulation. They evaluated the role of bone hormones in male reproduction. The review approach was structured around key hormonal pathways and their physiological effects.

Main Results:

Osteocytes produce sclerostin and RANKL, which regulate bone remodeling. These cells also secrete phosphatonins like FGF23 and active vitamin D. FGF23 influences phosphate metabolism and vitamin D levels. Osteoblasts secrete osteocalcin, which acts on multiple organs. Osteocalcin interacts with GPRC6A receptors in various tissues. This interaction modulates energy metabolism and male reproductive functions. The review highlights the role of bone hormones in chronic kidney disease. These findings suggest a broader endocrine role for bone beyond skeletal health.

Conclusions:

The authors synthesize evidence that bone functions as an endocrine organ. They emphasize the role of osteocytes and osteoblasts in hormone production. Bone-derived hormones influence phosphate and energy homeostasis. These hormones also affect male reproductive systems. The review suggests that bone hormones modulate kidney and parathyroid functions. The interaction with vitamin D and phosphates is a key finding. The authors propose that bone hormones have systemic effects beyond bone remodeling. This synthesis supports the need for further exploration of these hormonal pathways.

Osteocytes produce sclerostin and RANKL to regulate bone remodeling. They also secrete phosphatonins like FGF23 and active vitamin D.

Osteocalcin interacts with GPRC6A receptors in the pancreas, muscle, adipose tissue, brain, and testes.

FGF23 regulates phosphate excretion in the kidney and controls vitamin D metabolism.

Osteoblasts produce osteocalcin, which modulates energy and reproductive functions.

FGF23 and active vitamin D influence phosphate and vitamin D metabolism in kidney disease.

The authors suggest that bone hormones have systemic effects beyond skeletal regulation.