Can bones offer new hope for diabetes?
Research shows that the molecule osteocalcin, produced by bone cells, may help to regulate blood glucose levels.
Researchers at Columbia University found that increased levels of osteocalcin in mice both stimulated the insulin-producing cells in the pancreas and increased insulin sensitivity.
The researchers will now investigate the role of osteocalcin in regulating blood glucose in humans.
Matt Hunt, Science Information Manager at Diabetes UK, said: “This is a very interesting study.
“Diabetes research has never previously proposed the idea of the skeleton being involved in the development of diabetes. This could potentially open up a whole new area of research.
“Diabetes UK welcomes research which could lead to a better understanding of the causes of the condition. However, this research is in its very early stages and much more needs to be done before we can establish a conclusive link between osteocalcin in bones and diabetes. We look forward to further results.
“Diabetes affects over 2.2 million people in the UK and can lead to devastating complications such as blindness, heart disease, kidney failure and amputations.”
The research is published in the journal Cell.
http://download.cell.com/pdfs/0092-8674/PIIS0092867407007015.pdf
SUMMARY
The regulation of bone remodeling by an adipocyte-
derived hormone implies that bone may
exert a feedback control of energy homeostasis.
To test this hypothesis we looked for genes
expressed in osteoblasts, encoding signaling
molecules and affecting energy metabolism.
We show here that mice lacking the protein tyrosine
phosphatase OST-PTP are hypoglycemic
and are protected from obesity and glucose
intolerance because of an increase in b-cell
proliferation, insulin secretion, and insulin
sensitivity. In contrast, mice lacking the osteoblast-
secreted molecule osteocalcin display
decreased b-cell proliferation, glucose intolerance,
and insulin resistance. Removing one
Osteocalcin allele from OST-PTP-deficient
mice corrects their metabolic phenotype. Ex
vivo, osteocalcin can stimulate CyclinD1 and
Insulin expression in b-cells and Adiponectin,
an insulin-sensitizing adipokine, in adipocytes;
in vivo osteocalcin can improve glucose tolerance.
By revealing that the skeleton exerts an
endocrine regulation of sugar homeostasis
this study expands the biological importance
of this organ and our understanding of energy
metabolism.
