Bone mass may be directly related to metabolic health
According to two recent studies that are published in this month's edition of Cell
, there may be a key molecular link between bone remodeling and metabolism. Researchers found evidence that bone acts as an endocrine organ through the release of osteocalcin hormone, which causes cells in the pancreas to produce insulin.
They discovered that osteoblasts - cells that are responsible for bone formation - bear insulin receptors, and when treated with insulin show signs of collagen synthesis and glucose absorption.
Thomas Clemens, lead author of the study from Johns Hopkins University, found that mice whose bones cannot respond to insulin began to gain weight. They showed changes in their biochemistry that were consistent with insulin resistance. The mice also had low osteocalcin levels and fewer osteoblasts to produce bone. However, those symptoms improved with osteocalcin treatment.
The findings suggest that a drug that targets the bone in the same way that osteocalcin does might hold promise in fighting type 2 diabetes, according to the researchers.
Gerard Karsenty of Columbia University, lead author of the second study, explains that bone-building osteoblasts actually control bone resorption by osteoclasts, a process that takes place under very acidic conditions. Those conditions would also favor the chemical process that is necessary to produce active osteocalcin.
"Osteoporotic patients treated with [bone resorption inhibitors] may be at risk of glucose intolerance," Karsenty added.