BACKGROUND

Until recently, communication from metabolism to bone was considered purely unidirectional, involving complex interactions among an adipocyte-derived factor (leptin), the sympathetic nervous system and neuropeptides. However, studies in animal models now show that bone regulates glucose metabolism and fat mass via the uncarboxylated form of an osteoblast-derived factor (osteocalcin). These findings not only demonstrate that energy metabolism regulates bone remodeling through neural relays, but also that the skeleton acts as an endocrine tissue that regulates metabolic homeostasis.

CONCLUSIONS

Further study is needed to understand the physiological role of these complex interactions in man and their implications for human diseases.