When the body fails to regulate blood sugar (glucose), it may result in serious, and even fatal, complications like diabetes. The regulation of glucose is a function of not one, but three organs of the body, namely the pancreas, the liver, and the muscles, with some help from fats. However, a startling new discovery about a hormone released from the bone is significantly changing our understanding of diabetes and giving new clues on how to deal with it.
Diabetes is considered to be the fifth leading killer of Americans. In addition to the body's failure to regulate glucose, other specific types of diabetes result from specific genetic syndromes, surgery, drugs, malnutrition, infections, and other illnesses.
On the other hand, new research suggests that the issue is even more complex than what it seems to be. A hormone from the skeleton may influence how the body handles sugar. There is also increasing evidence that demonstrates that the signals from the immune system, the brain, and the gut play very important roles in controlling glucose and lipid metabolism. These findings are mainly relevant to Type 2 diabetes, the more common kind, which comes on in adulthood.
While elevated blood sugar defines diabetes, the reasons for abnormal sugar tend to be different from one individual to another. It is in understanding exactly what signals are involved that raises the hope of providing the right care for each person each day, rather than giving everyone the same drug.
Lead researcher, Dr. Gerard Karsenty, first described the findings at a conference where the assembled scientists appeared to be overwhelmed by the potential implications of the study. It was the first time that the skeleton was actually seen as an endocrine organ, producing hormones that act outside of bone.
In his previous work, he had shown that a hormone produced by fat, called leptin, is an important regulator of bone metabolism. In this work, idea that if fat regulates bone, bone must regulate fat was tested. His experiment with mice revealed that a previously known substance called osteocalcin, which is produced by bone, acted by signaling fat cells, as well as the pancreas. The net effect is to improve how mice secrete and handle insulin, the hormone that helps the body move glucose from the bloodstream into cells of the muscle and liver, where it can be used for energy or stored for future use. Insulin is also important in regulating lipids.
Patients with Type 2 diabetes no longer heed the hormone’s directives due to the cells' resistance to insulin. Their blood glucose levels surge and production of insulin in the pancreas decline as well.
The experiment revealed an increase in osteocalcin which addressed the twin problems of insulin resistance and low insulin production. The mice became more sensitive to insulin and it increased their insulin production, thus bringing their blood sugar down. As a bonus, it also made obese mice less fat.
Should osteocalcin works in humans as well, it can be considered as a “unique new treatment” for Type 2 diabetes. Most current diabetes drugs either raise insulin production or improve insulin sensitivity, but not both. Drugs that increase production tend to make insulin resistance worse. A deficiency in osteocalcin could also turn out to be a cause of Type 2 diabetes.
Diabetes is considered to be the fifth leading killer of Americans. In addition to the body's failure to regulate glucose, other specific types of diabetes result from specific genetic syndromes, surgery, drugs, malnutrition, infections, and other illnesses.
On the other hand, new research suggests that the issue is even more complex than what it seems to be. A hormone from the skeleton may influence how the body handles sugar. There is also increasing evidence that demonstrates that the signals from the immune system, the brain, and the gut play very important roles in controlling glucose and lipid metabolism. These findings are mainly relevant to Type 2 diabetes, the more common kind, which comes on in adulthood.
While elevated blood sugar defines diabetes, the reasons for abnormal sugar tend to be different from one individual to another. It is in understanding exactly what signals are involved that raises the hope of providing the right care for each person each day, rather than giving everyone the same drug.
Lead researcher, Dr. Gerard Karsenty, first described the findings at a conference where the assembled scientists appeared to be overwhelmed by the potential implications of the study. It was the first time that the skeleton was actually seen as an endocrine organ, producing hormones that act outside of bone.
In his previous work, he had shown that a hormone produced by fat, called leptin, is an important regulator of bone metabolism. In this work, idea that if fat regulates bone, bone must regulate fat was tested. His experiment with mice revealed that a previously known substance called osteocalcin, which is produced by bone, acted by signaling fat cells, as well as the pancreas. The net effect is to improve how mice secrete and handle insulin, the hormone that helps the body move glucose from the bloodstream into cells of the muscle and liver, where it can be used for energy or stored for future use. Insulin is also important in regulating lipids.
Patients with Type 2 diabetes no longer heed the hormone’s directives due to the cells' resistance to insulin. Their blood glucose levels surge and production of insulin in the pancreas decline as well.
The experiment revealed an increase in osteocalcin which addressed the twin problems of insulin resistance and low insulin production. The mice became more sensitive to insulin and it increased their insulin production, thus bringing their blood sugar down. As a bonus, it also made obese mice less fat.
Should osteocalcin works in humans as well, it can be considered as a “unique new treatment” for Type 2 diabetes. Most current diabetes drugs either raise insulin production or improve insulin sensitivity, but not both. Drugs that increase production tend to make insulin resistance worse. A deficiency in osteocalcin could also turn out to be a cause of Type 2 diabetes.
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