Two things have changed for many people with type 2 diabetes.
The first is that their blood glucose levels are lower than they were five years ago.
The second is that the condition has been steadily increasing in number.
In the past decade, there has been an explosion of research into ways to control this autoimmune disease, and now researchers have developed a new method to do just that.
They’ve developed a gene that works by stopping the body from building up a new protein called insulin.
It’s an interesting gene because the protein that it blocks is responsible for insulin’s ability to work, and because it is already present in the pancreas, it is one of the most common and effective treatments for type 2.
“We’ve been able to produce this gene for about two years, and we’re just now getting into the next phase,” said Dr. Scott Miller, an associate professor of medicine at Stanford University School of Medicine and director of the Diabetes Research Center.
Miller and his colleagues have tested it in mice with a gene mutation that causes a condition called interleukin-6.
When the mutation is present, it causes interleukem-derived antibodies, a group of antibodies that attack the cells lining the blood vessels of the body.
These antibodies are usually harmless.
But when the mutation in interleucin-1 causes antibodies to attack these vessels, it produces an immune response that attacks the cells, destroying them.
These immune responses are the main reason that people with diabetes develop arthritis and other joint problems.
The scientists have developed another gene that blocks interleu-6 antibodies.
They hope that the other gene will block the interleuca-1 response as well, which could help people with Type 2 with more manageable arthritis.
“There’s a huge potential here,” Miller said.
In this study, researchers isolated a gene encoding a protein that controls interleus-6, and they gave mice a cocktail of compounds, including one that blocks the interferon-beta receptor, or FvB, a protein found on cells lining blood vessels, to induce arthritis in the mice.
The results were impressive.
Mice that received a cocktail containing an antibody blocking FvC or a gene called FvA3 were more likely to develop arthritis than mice that didn’t get a treatment.
When it came to the effect of the cocktail on the arthritis itself, the mice who received the treatment were almost twice as likely to have the disease as the control mice.
Miller is hopeful that the drug could be tested in humans, as it could help the millions of people who don’t have the gene mutation, but he and his team are still testing whether the drug works in other people with the same mutation.
One thing that he hopes is that people will learn more about the gene before they begin to take the drug.
“If you can figure out a way to target this protein, then it’s going to be a huge boon to people with other conditions like Type 2, because it’s a big part of their arthritis and they want to be able to control it,” he said.
It took nearly a decade for the scientists to develop the gene, and in some cases, it took years to find a suitable treatment for their mutation.
But now, they are getting the gene to a person in a clinical trial.
“It’s a good thing, because the gene is still very rare,” Miller told FourFourtwo.
“So this is a really good step forward.”
The first gene to be tested was the interlesuins-1 gene.
“This gene was isolated in 2001, and it’s been tested in mice for several years now,” Miller explained.
“The problem with the gene was that it’s found only in mice.
So there were a lot of problems that had to be solved before we could begin to use it.”
Miller’s team tested the gene in mice and in humans.
They found that interleufins-2 (also known as interleuceins-3), a protein made by the immune system, was the most effective treatment.
That’s a sign that the interlexus proteins are actually important for the immune response, Miller said, because they protect the cells from attacks from invaders.
And he said that finding a gene for the interlineucins-4 protein could provide another way to treat Type 2 diabetes, because that protein is known to be involved in intercellular signaling, or the interaction of cells.
“Interleukins-5, which are a family of proteins that regulate the activity of the immune responses in cells, have also been shown to play a role in the control of the intercellumular signaling that is essential for the development of Type 2,” Miller added.
“These proteins have also shown to be important for regulating the intermeiotic signaling that controls the activity in cells.”
Researchers are now developing another gene to block interleutins-6 in mice, and another to block the immune-related interle