Type 1 Diabetes: No More Insulin?

(Ivanhoe Newswire) — About 1 million people are affected by type 1 diabetes in the United States. According to a new study, type 1 diabetes could be converted to an asymptomatic, non-insulin dependent disorder by eliminating the actions of a specific hormone.

Type 1 diabetes is typically first diagnosed in children and teenagers. It is a disease where the body doesn’t produce insulin — a hormone that is needed to convert sugars, starches, and other food into energy.

Glucagon is a hormone secreted by the pancreas that prevents low blood sugar in healthy people. It causes high blood sugar in people with type 1 diabetes. The study done on mice suggests that insulin is unnecessary, and its absence doesn’t cause diabetes or any other abnormality when the actions of glucagon are suppressed, meaning that the elimination of glucagon action restores glucose tolerance to normal.

“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,” Dr. Roger Unger, professor of internal medicine and senior author of the study, was quoted as saying. “If diabetes is defined as restoration of glucose homeostasis to normal, then this treatment can perhaps be considered very close to a ‘cure.’ “

Normally, glucagon is released when the glucose, or sugar, level in the blood is low. In insulin deficiency, however, glucagon levels are inappropriately high and cause the liver to release excessive amounts of glucose into the bloodstream. This action is opposed by insulin, which directs the body’s cells to remove sugar from the bloodstream.

In this study, UT Southwestern scientists tested how mice engineered to lack working glucagon receptors responded to an oral glucose tolerance test. The test measures the body’s ability to metabolize, or clear, glucose from the bloodstream.

The results showed that the mice with normal insulin production, but without functioning glucagon receptors, responded normally to the test. The mice also responded normally when their insulin-producing beta cells were destroyed. The mice had no insulin or glucagon action, but they did not develop diabetes.

“And if you don’t have glucagon, then you don’t need insulin,” Dr. Unger, who is also a physician at the Dallas VA Medical Center, was quoted as saying.

Dr. Young Lee, assistant professor of internal medicine at UT Southwestern and lead author of the study, said the next step is to determine the mechanism behind this result.

“Hopefully, these findings will someday help those with type 1 diabetes,” 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.”

“Matching the high insulin levels needed to reach glucagon cells with insulin injections is possible only with amounts that are excessive for other tissues,” Dr. Unger 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.”

SOURCE: Diabetes, published online January 26, 2011

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