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Research shows skeleton to be endocrine organ
http://www. physorg. com/ news105890812. html
August 09, 2007
Bones are typically considered calcified, inert tissues, but researchers at Columbia University Medical Center have now identified a surprising and crucial new function of bones.
They have demonstrated for the first time that bones are an endocrine organ, aiding in the regulation of our sugar metabolism, body weight, and, consequently, are a major determinant in the development of type 2 diabetes.
This research, published in the August 10 issue of Cell, shows that bone cells release a hormone called osteocalcin, which controls blood sugar (glucose) regulation and fat deposition through previously unknown synergistic mechanisms.
Typically, an increase in insulin secretion is accompanied by a decrease in insulin sensitivity. However, osteocalcin increases both insulin secretion and sensitivity, while also boosting the number of insulin-producing cells and reducing fat accumulation.
In the published study, the authors demonstrated that increased osteocalcin activity prevents mice from developing type 2 diabetes and obesity. This discovery could open the door to novel therapies for preventing and treating type 2 diabetes.
"Our bones, in ways previously unknown, are responsible for regulating blood sugar, a finding that completely changes our understanding of bone function and reveals important aspects of energy metabolism," said Gerard Karsenty, M.D., Ph.D., chair of the Department of Genetics and Development at Columbia University Medical Center, the Paul Marks Professor in Basic Science, and senior author of the paper. "These results reveal an important aspect of endocrinology that was previously unappreciated until now."
Karsenty and his colleagues previously demonstrated that leptin, a hormone released by fat cells, acts on bone mass and ultimately controls bone mass. They therefore 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.
The researchers discovered osteocalcin, a protein made only by bone-forming cells (osteoblasts), which is not only a structural protein but also a hormone with entirely unexpected and important functions. Osteocalcin directs the pancreas's beta cells, which produce the body's supply of insulin, to produce more insulin. At the same time, osteocalcin directs fat cells to release a hormone called adiponectin, which increases insulin sensitivity. This discovery is the first to demonstrate that a single hormone can have a synergistic function in regulating both insulin secretion and insulin sensitivity, and that this coordinated signal originates from bones. Furthermore, osteocalcin enhances the production of insulin-producing beta cells, which is considered one of the best, yet currently unattainable, strategies for diabetes treatment.People with type 2 diabetes often show low levels of osteocalcin, suggesting that altering the activity of this molecule could be an effective therapy. This hypothesis is supported by research from Columbia University, which demonstrated that mice with high levels of osteocalcin activity could avoid becoming overweight or developing diabetes, even when fed a high-fat diet.
Analysis of mice lacking osteocalcin confirmed the presence of type 2 diabetes, increased lipids, reduced insulin, decreased adiponectin expression, and reduced β-cell proliferation.
This research was supported by the NIH, the American Diabetes Association, the Japan Society for the Promotion of Science, and the Pennsylvania Department of Health.
Researchers are currently examining the role of osteocalcin in blood sugar control in humans and continuing to investigate the relationship between osteocalcin, type 2 diabetes, and obesity.
Source: http://www. wretch. cc/ blog/ fsj/ 8405829
Study: Bones Act as Endocrine Organs Regulating Diabetes and Obesity
http://www. physorg. com/ news105890812. html
August 09, 2007
Bones are typically considered calcified, inert tissues, but researchers at Columbia University Medical Center have now identified a surprising and crucial new function of bones.
They have demonstrated for the first time that bones are an endocrine organ, aiding in the regulation of our sugar metabolism, body weight, and, consequently, are a major determinant in the development of type 2 diabetes.
This research, published in the August 10 issue of Cell, shows that bone cells release a hormone called osteocalcin, which controls blood sugar (glucose) regulation and fat deposition through previously unknown synergistic mechanisms.
Typically, an increase in insulin secretion is accompanied by a decrease in insulin sensitivity. However, osteocalcin increases both insulin secretion and sensitivity, while also boosting the number of insulin-producing cells and reducing fat accumulation.
In the published study, the authors demonstrated that increased osteocalcin activity prevents mice from developing type 2 diabetes and obesity. This discovery could open the door to novel therapies for preventing and treating type 2 diabetes.
"Our bones, in ways previously unknown, are responsible for regulating blood sugar, a finding that completely changes our understanding of bone function and reveals important aspects of energy metabolism," said Gerard Karsenty, M.D., Ph.D., chair of the Department of Genetics and Development at Columbia University Medical Center, the Paul Marks Professor in Basic Science, and senior author of the paper. "These results reveal an important aspect of endocrinology that was previously unappreciated until now."
Karsenty and his colleagues previously demonstrated that leptin, a hormone released by fat cells, acts on bone mass and ultimately controls bone mass. They therefore 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.
The researchers discovered osteocalcin, a protein made only by bone-forming cells (osteoblasts), which is not only a structural protein but also a hormone with entirely unexpected and important functions. Osteocalcin directs the pancreas's beta cells, which produce the body's supply of insulin, to produce more insulin. At the same time, osteocalcin directs fat cells to release a hormone called adiponectin, which increases insulin sensitivity. This discovery is the first to demonstrate that a single hormone can have a synergistic function in regulating both insulin secretion and insulin sensitivity, and that this coordinated signal originates from bones. Furthermore, osteocalcin enhances the production of insulin-producing beta cells, which is considered one of the best, yet currently unattainable, strategies for diabetes treatment.People with type 2 diabetes often show low levels of osteocalcin, suggesting that altering the activity of this molecule could be an effective therapy. This hypothesis is supported by research from Columbia University, which demonstrated that mice with high levels of osteocalcin activity could avoid becoming overweight or developing diabetes, even when fed a high-fat diet.
Analysis of mice lacking osteocalcin confirmed the presence of type 2 diabetes, increased lipids, reduced insulin, decreased adiponectin expression, and reduced β-cell proliferation.
This research was supported by the NIH, the American Diabetes Association, the Japan Society for the Promotion of Science, and the Pennsylvania Department of Health.
Researchers are currently examining the role of osteocalcin in blood sugar control in humans and continuing to investigate the relationship between osteocalcin, type 2 diabetes, and obesity.
Source: http://www. wretch. cc/ blog/ fsj/ 8405829