Okay, it’s in the mouse stage, but it looks interesting nonetheless. If this turns out to be a totally new knowledge area it could make some pieces of the puzzle start to fit together a bit better:
Bones are typically thought of as calcified, inert structures, but researchers at Columbia University Medical Center have now identified a surprising and critically important novel function of the skeleton. They’ve shown for the first time that the skeleton is an endocrine organ that helps control our sugar metabolism and weight and, as such, is a major determinant of the development of type 2 diabetes.
The research, published in the August 10 issue of Cell, demonstrates that bone cells release a hormone called osteocalcin, which controls the regulation of blood sugar (glucose) and fat deposition through synergistic mechanisms previously not recognized. Usually, an increase in insulin secretion is accompanied by a decrease in insulin sensitivity. Osteocalcin, however, increases both the secretion and sensitivity of insulin, in addition to boosting the number of insulin-producing cells and reducing stores of fat.
In this published research, authors show that an increase in osteocalcin activity prevents the development of type 2 diabetes and obesity in mice. This discovery potentially opens the door for novel therapeutic avenues for the prevention and treatment of type 2 diabetes.
“The discovery that our bones are responsible for regulating blood sugar in ways that were not known before completely changes our understanding of the function of the skeleton and uncovers a crucial aspect of energy metabolism,” said Gerard Karsenty, M.D., Ph.D., chair of the department of Genetics and Development at Columbia University Medical Center, Paul Marks Professor in the Basic Sciences, and senior author of the paper. “These results uncover an important aspect of endocrinology that was unappreciated until now.”
Karsenty and his colleagues had previously shown that leptin, a hormone released by fat cells, acts upon and ultimately controls bone mass. They reasoned that bones must in turn communicate with fat, so they searched bone-forming cells for molecules that could potentially send signals back to fat cells.