However, 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 an 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 during adulthood.
While it is true that having elevated blood sugar is the defining feature of 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.
When researchers from Columbia University Medical Center published the results last summer, scientists were astounded that a hormone released from the bone may help regulate blood glucose. 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, he tested the idea that if fat regulates bone, bone in essence must regulate fat. His experiment with mice revealed that a previously known substance called osteocalcin, which is produced by bone, acted by sending signals to the 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 declines 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.
The immune system is considered to be another cause of glucose regulation. In 2003, researchers from two laboratories found that fat tissue from obese mice contained an abnormally large number of macrophages, immune cells that contribute to inflammation.
Scientists have long suspected that inflammation was somehow related to insulin resistance, which precedes nearly all cases of Type 2 diabetes. In the early 1900s, diabetics were sometimes given high doses of aspirin, which is an anti-inflammatory. Only in the past few years has research into the relationship of obesity, inflammation and insulin resistance become a serious concern.
A number of researchers agree that obesity is accompanied by a state of chronic, low-grade inflammation in which some immune cells are activated, which may be a primary cause of insulin resistance. They also agree that the main type of cell responsible for the inflammation is the macrophage.
Should more research prove the initial findings to be true, there would be certainly greater hope of relief and treatment for diabetics everywhere.
