Scientists have discovered a treatment that could potentially transform type 1 diabetes into a condition that produces no symptoms and does not require regular insulin injections.
The breakthrough centres on glucagon, a hormone produced in the pancreas that prevents low blood sugar levels in healthy individuals but causes high blood sugar in people with type 1 diabetes.
Normally glucagon is produced when blood sugar (glucose) levels are low, but when an individual lacks enough insulin, the glucagon levels will be too high, resulting in the liver releasing excessive amounts of glucose into the bloodstream. Insulin injections are used to redress this imbalance.
The researchers, from UT Southwestern Medical Center in Dallas, found that mice who are genetically altered to prevent the action of glucagon and are also unable to produce insulin are still able to clear glucose from the blood stream – i.e. they do not have the symptoms of diabetes.
Diabetes
Commenting on the findings, study leader Dr Roger Unger said: “These findings suggest that if there is no glucagon, it doesn’t matter if you don’t have insulin. 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.”
In fact, the treatment restores glucose tolerance to normal, something that insulin injections cannot do.
The treatment could be of enormous benefit because, aside from the cost and inconvenience, insulin injections require doses much higher than the body needs – this is to ensure that enough insulin gets to the right parts of the body – and these levels can be damaging to other body tissues.
“If these latest findings were to work in humans, injected insulin would no longer be necessary for people with type 1 diabetes” Dr Unger said.
The next step is to determine the exact mechanism behind the results. The study is published in the February issue of Diabetes.
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Researchers at Washington University School of Medicine in St. Louis have identified a key mechanism that appears to contribute to blood vessel damage in people with diabetes.
The researchers said studies in mice show that the damage appears to involve two enzymes, fatty acid synthase (FAS) and nitric oxide synthase (NOS), that interact in the cells that line blood vessel walls.
“We already knew that in diabetes there’s a defect in the endothelial cells that line the blood vessels,” said first author Xiaochao Wei.
“People with diabetes also have depressed levels of fatty acid synthase. But this is the first time we’ve been able to link those observations together.”
Wei studied mice that had been genetically engineered to make FAS in all of their tissues except the endothelial cells that line blood vessels. These so-called FASTie mice experienced problems in the vessels that were similar to those seen in animals with diabetes.
“It turns out that there are strong parallels between the complete absence of FAS and the deficiencies in FAS induced by lack of insulin and by insulin resistance,” Clay F. Semenkovich, the Herbert S. Gasser Professor of Medicine, professor of cell biology and physiology and chief of the Division of Endocrinology, Metabolism and Lipid Research said.
Comparing FASTie mice to normal animals, as well as to mice with diabetes, Wei and Semenkovich determined that mice without FAS, and with low levels of FAS, could not make the substance that anchors nitric oxide synthase to the endothelial cells in blood vessels.
“We’ve known for many years that to have an effect, NOS has to be anchored to the wall of the vessel,” Semenkovich said.
“Xiaochao discovered that fatty acid synthase preferentially makes a lipid that attaches to NOS, allowing it to hook to the cell membrane and to produce normal, healthy blood vessels.”
In the FASTie mice, blood vessels were leaky, and in cases when the vessel was injured, the mice were unable to generate new blood vessel growth.
The actual mechanism involved in binding NOS to the endothelial cells is called palmitoylation. Without FAS, the genetically engineered mice lose NOS palmitoylation and are unable to modify NOS so that it will interact with the endothelial cell membrane. That results in blood vessel problems.
It’s a long way, however, from a mouse to a person, so the researchers next looked at human endothelial cells, and they found that a similar mechanism was at work.
“Our findings strongly suggest that if we can use a drug or another enzyme to promote fatty acid synthase activity, specifically in blood vessels, it might be helpful to patients with diabetes,” Wei said.
The study has been published in the Journal of Biological Chemistry.