Type 1 Cure in the Making?
Those with Type 1 diabetes can continue to hope for a cure for their condition in the near future. New findings by the University of Texas Southwestern Medical Center have found a way to convert the dreaded condition into an asymptomatic, non-insulin dependent disorder.
According to the study, this can theoretically be done by inhibiting the activity of a specific hormone. The hormone is Glucagon and this is produced in the pancreas. Its primary function is to prevent low blood sugar levels in healthy individuals. In individuals with Type 1 diabetes though, it causes high blood sugar.
By inhibiting the activity of glucagon, insulin becomes unneeded by the individual with Type 1 diabetes. The absence of the hormone produces no ill effects such as onset diabetes or any other abnormality.
All these were found when studies using laboratory mice were used. According to Dr. Roger Unger, Professor of Internal Medicine and senior author of the study said, “We’ve all been brought up to think insulin is the all-powerful hormone without which life is impossible, but that isn’t the case.”
The study would be published in the February issue of Diabetes. He added that “If diabetes is defined as restoration of glucose homeostasis to normal, then this treatment can perhaps be considered very close to a ‘cure.’ ”
For many generations, insulin treatment has been the norm for the management of Type 1 diabetes in humans since 1922. Even at optimal management of Type 1 diabetes, the hormone insulin by itself cannot restore the failed glucose tolerance mechanism of the body. These findings suggest that by eliminating glucagons activity, the glucose management system can be restored allowing for normal tolerances of blood sugar in the body.
Glucagon is normally produced by the pancreas when blood sugar is low. However, due to insulin deficiency, glucagons levels are inordinately high which results in the liver to compensate by introducing glucose into the bloodstream. This is counteracted through the injection of insulin, which directs the cells to remove the excess sugar from the bloodstream. The laboratory research of Dr. Unger found that insulin’s benefit results from the hormones suppression of glucagon.
About one million individuals are afflicted with Type 1 diabetes in the United States. In this condition, the pancreatic islet cells, the cells that produce insulin, are non-functional. To compensate for this condition, these individuals ingest insulin several times a day to be able to metabolize blood sugar, manage sugar levels and avoid diabetic coma. Their diets are also severely restricted to prevent sudden spikes in their blood sugar levels.
The study tested genetically altered mice respond to an oral glucose test. The mutation in the mice is that they do not have working glucagon receptors in their bodies. This test is often used to diagnose pre-diabetes, gestational diabetes and diabetes itself and it measures the body’s ability to metabolize excess glucose from the bloodstream.
The scientists from UT Southwestern found that the mice that produce normal insulin without the glucagons receptors responded normally to the test. These mice also yielded normal test results when their insulin producing beta cells were destroyed. Without insulin or glucagons producing cells in their bodies, these mice still did not develop diabetes.
“These findings suggest that if there is no glucagon, it doesn’t matter if you don’t have insulin,” said Dr. Unger, who is also a physician at the Dallas VA Medical Center. “This does not mean insulin is unimportant. It is essential for normal growth and development from neonatal to adulthood. But in adulthood, at least with respect to glucose metabolism, the role of insulin is to control glucagon.”
“And if you don’t have glucagon, then you don’t need insulin,” added Dr. Young Lee, Assistant Professor of Internal Medicine at UT Southwestern. The next goal is to determine the process that can produce these same results in humans. Dr. Lee said. “If we can find a way to block the actions of glucagon in humans, then maybe we can minimize the need for insulin therapy.”
Dr. Unger said anything that reduces the need for injected insulin is a positive. ”Matching the high insulin levels needed to reach glucagon cells with insulin injections is possible only with amounts that are excessive for other tissues,” he said. “Peripherally injected insulin cannot accurately duplicate the normal process by which the body produces and distributes insulin. If these latest findings were to work in humans, injected insulin would no longer be necessary for people with type 1 diabetes.”
The study was funded in part by the VA North Texas Health Care System, the American Diabetes Association and the National Institutes of Health.