Strong synergy is the key- combining a vaccine and an immunosuppressant drug:

Scientists have used a two-pronged treatment to reverse recent-onset type 1 diabetesdiabetes in mice.
The approach hasn’t yet been tested on humans, but the results from tests on mice are “encouraging,” the researchers write in The Journal of Clinical Immunology.

The scientists gave mice oral doses of antibodies that targeted certain immune system cells, called T cells, that are involved in attacking pancreatic cells in type 1 diabetes. After slowing down the immune system’s attack on insulin cells, the researchers gave the mice intranasal doses of a peptide (a building block of protein) that boosted protection of the insulin-producing pancreatic cells.
The danger of suppressing the immune system is that it puts patients at increased risk of cancers or viral infections. But by combining drugs, a lower dose of the immuno-suppressant antibody is required, with a lower risk of side effects.
Encouraging but: has only been tried on mice, works only on those with Type 1, may have negative side effects, must go through FDA approval, etc. We look forward to learing more.

Insulin resistance, the predecessor to Type 2 Diabetes, relates to the ineffectiveness of the insulin hormone to transfer glucose into the body’s cells to be used as fuel. In particular, insulin binds to a spot on the cell surface called a receptor. Likened to a lock and key, insulin is the key that opens up the lock (receptor) so that glucose can pass through the door into the cell. Using this analogy in Type 1 diabetes, the keys have been stolen (no insulin is made by the pancreas). In Type 2, the door won’t open fully even with the right key (insulin resistance). [Source: FDA]
Although there has been a lot of emphasis on lifestyle and nutritional risk factors which influence the onset of the disease, fundamental questions remain regarding what actually causes Type 2 diabetes. For example, why do some individuals, who are do not have lifestyle risk factors, become diabetic? And, what causes insulin to be ineffective?
Physiologist Gerald Shulman and his colleagues at Yale University took on these questions in a study of 20-year-olds whose parents are diabetic. Despite being young, healthy and lean, all of the test subjects had high levels of insulin resistance:

Insulin resistance is often referred to as “pre-diabetes” because it’s the first sign that the body is not processing sugar properly.
After eating a meal, the digestive system breaks most food down into units of glucose, a simple sugar that is one of the basic energy sources for the body. Insulin is a hormone made by the pancreas, which triggers cells to absorb the glucose and use it. Once inside the cell, small energy factories called mitochondria convert the glucose sugar into a chemical called ATP. ATP powers every cellular and bodily function, from thinking to moving. When someone is insulin resistant, his or her cells aren’t able to absorb sugar from the bloodstream to make ATP, which leaves the cells starving for energy even though it’s right there just outside the cell wall.

Interestingly, although the study participants were lean, they had more fat inside their muscle cells than is typical.

Shulman says, “Fat inside the muscle cell causes insulin resistance; so the real question becomes, ‘Why is the fat building up?’ … So it became a question of, are there defects in the fat cells in the body, releasing more fat to liver and muscle, causing the buildup? Or are there defects in the mitochondria… the factories in all the cells of our body that produce energy?”

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A study led by researchers at Beth Israel Deaconess Medical Center (BIDMC) has shown that a protein found in fat cells is a newly discovered cause of insulin resistance, establishing a previously unidentified molecular link between obesity and type 2 diabetes and offering a potential new target for the development of drugs to treat diabetes. The findings appear in the July 21 issue of the journal Nature.

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In type 1 diabetes, which by definition indicates a lack of insulin production, the insulin-producing “beta” cells in the pancreas are thought to be wiped out. At least, this was the common understanding until a new study provided evidence that the human pancreas continues to form beta cells even in individuals who have had type 1 diabetes for may years.
“The implication is that type 1 diabetes could, theoretically, be cured if we could stop the new insulin-secreting cells being destroyed,” Dr. Peter C. Butler from the University of California in Los Angeles told Reuters Health. Butler presented his team’s findings at the American Diabetes Association’s annual meeting in San Diego.
Read more here

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NEW YORK (Reuters Health) – Experiments in rats suggest that minocycline, an antibiotic, could curb a common cause of vision problems in people with diabetes.
Minocycline is a “strong candidate for further consideration as a therapeutic drug in reducing the retinal complications of diabetes,” Dr. J. Kyle Krady and colleagues from the Pennsylvania State University College of Medicine in Hershey write in the medical journal Diabetes.
Recent evidence has suggested that diabetes leads to ongoing inflammatory activity within the retina, Krady explained. Immune cells called microglia are the main sources of inflammation in the retina, and “therefore represent an important target for reducing this inflammation.”

BOSTON–(BUSINESS WIRE)–May 23, 2005–Joslin Diabetes Center scientists have discovered a group of genes that govern the genesis of calorie-burning fat cells. This discovery may lead to novel ways to treat obesity in humans.
“With obesity at epidemic levels, finding new ways to treat it is one of medicine’s holy grails,” said C. Ronald Kahn, M.D., President of Joslin Diabetes Center, the Mary K. Iacocca Professor of Medicine at Harvard Medical School (HMS), and principal investigator of the study that appears in the June edition of the journal Nature Cell Biology. In laboratory studies of mouse cells, his research team identified genes that govern how precursor cells give rise to mature brown fat cells. There are two main types of fat cells in the body — white and brown. White fat cells are the “conventional” form of fat that we all recognize. They are designed to store energy for use in times of need. Chocked full of lipid droplets, these big cells accumulate under the skin and around internal organs.

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From NewHopeBlog:
Results of a recent study offer new hope for novel treatment options in diabetes. Scientists have successfully modified liver cells to produce insulin that, when transplanted into mice, brought diabetes under control.

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News Release: Scientists at the Weizmann Institute of Science, Israel, and in Sweden Discover How Excess Body Fat Can Lead to the Onset of Diabetes
One out of 12 people in the western world suffers from type 2 (adult onset) diabetes. Worldwide, 150 million people are diabetic and their numbers are expected to double in the next 20 years, a result of the growing obesity epidemic. Yet, the reasons for the strong correlation between excess body fat and diabetes have been puzzling researchers. Scientists at the Weizmann Institute of Science and the University of Umea, Sweden, have now unraveled a mechanism by which fat contributes to the onset of the disease. Their results were published in the April issue of Cell Metabolism.

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NewHopeBlog has published more information related to a report about the mechanisms leading to Type I diabetes:

The results of long-term studies indicate that insulin is the trigger that unleashes autoimmune lymphocytes to attack beta islet cells in the pancreas that produce insulin. Could a therapeutic approach to preventing the lymphocytes from attacking the beta islet cells [perhaps by a mechanism of CD8+(T-suppressor cell) activation] involve controlling NKT-cell activity – a hot target of current research in autoimmune diseases? Could ineffective NKT cell-mediated immunoregulation in autoimmune-prone individuals such as with nonobese diabetic (NOD) mice be related to defective signals that regulate CD1d(the NKT cell restriction molecule) expression at time and site of autoimmunity? Let’s look at the news report of the research indicating that insulin is the trigger, and you can see that these questions just might fit the article like OJ’s glove:

AFP via Yahoo
Researchers believe they have made an important breakthrough in understanding the severest form of diabetes, confirming that the disease begins when the body’s immune system reacts to the hormone insulin.
Type 1 diabetes usually occurs in childhood, when immune cells called lymphocytes start to attack beta islet cells that make insulin in the pancreas. A vicious circle then starts up. The remnants of the beta cells are transported to a draining lymph node in the pancreas, where they attract the attention of immune-system scouts, which in turn prime more lymphocytes to destroy more beta cells.
After 80-90 percent of the beta cells have been wiped out, the first clinical symptoms of diabetes show up.
The pioneering work by University of Colorado scientist George Eisenbarth and colleagues indicates that insulin is the trigger which unleashes autoimmune lymphocytes. The discovery throws up exciting avenues for potential treatment, perhaps by wiping out the aggressive cells or preventing them from going on the offensive in the first place, he said.
more …

Researchers believe they have made an important breakthrough in understanding the severest form of diabetes, confirming that the disease begins when the body’s immune system reacts to the hormone insulin.
Type 1 diabetes usually occurs in childhood, when immune cells called lymphocytes start to attack beta islet cells that make insulin in the pancreas.
The pioneering work by University of Colorado scientist George Eisenbarth and colleagues indicates that insulin is the trigger which unleashes autoimmune lymphocytes. The discovery throws up exciting avenues for potential treatment, perhaps by wiping out the aggressive cells or preventing them from going on the offensive in the first place, he said.
more

[Read more...]

Following ground-breaking research, US scientists believe they have found a way to use brain stem cells to “cure” diabetes. Although the work is not yet ready to be tested on human patients, results in animals have been promising, say the Stanford University researchers.
Many have conjectured stem cells harvested from human embryos could be used to treat diabetes, despite the known ethical issues and medical limitations (e.g., the development of tumors). Dr Seung Kim and colleagues looked at whether adult stem cells taken from the brain might work effectively and at the same time avoid the known obstacles associated with embryonic stem cells.
Dr Kim’s team added a cocktail of chemicals to brain stem cells and caused them to change and produce insulin in response to blood sugar levels.
To find out whether these cells would “work”, they transplanted them into a cavity in the kidney in mice where other types of insulin-producing cells have been found to survive before.
When the blood sugar went up in these mice, the transplanted “mature” brain stem cells again released insulin.
Four weeks later, the cells were still alive and producing insulin and none had turned cancerous.
One of the potential benefits of this treatment approach is each individual would be their own donor.
more here

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An islet cell transplant performed at Carolinas Medical Center in Charlotte, NC appears to have had success after three procedures:

Andrea Anderson is a transplant recipient, “It’s still hard to believe I’m off insulin, when I do tests with my meter, I mean I’m still doing that, and getting a level of 100 or 80 or 120, it’s amazing to me after I’ve just eaten, you know, maybe a bowl of spaghetti.”
For anyone with diabetes, what Anderson is describing is simply astounding. Dr. Paul Gores is a transplant surgeon, “It was apparent pretty much within 24 hours that this was gonna work.”
Gores says that was after Annie’s third pancreatic islet cell transplant, “We waited two weeks, and we measured her insulin secretion, and the islets, the secretion was beautiful. It was better than mine, I’m sure.”
Each of Annie’s transplants started inside a lab with a pancreas from an organ donor. Dr. Craig Halberstadt says for 14 hours, the transplant team separated out minute islet cells, “A thimbleful of cells that we could transplant back into the patient.”
more

A study conducted at the University of Buffalo (on rats) indicates that obesity and diabetes may be influenced by the maternal intrauterine environment. The researchers believe (of course) that their results can be extended to humans.

The adage “You are what you eat” should be rephrased to include “and so are your children,” based on metabolic research pioneered by researchers at the University at Buffalo.
Previous studies by the UB scientists showed that rat pups raised artificially on a high-carbohydrate milk formula identical in calories to mother’s milk developed changes in pancreatic islets, resulting in overproduction of insulin and obesity in adulthood.

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Previously, researchers discovered that adult stem cells taken from the spleen could regenerate the insulin-producing islets of the pancreas. The finding is significant because it provides a potential cure for diabetes.
The same team is now reporting that spleen adult stem cells have properties previously believed to be present only during the embryonic development of mammals [more].

“There may be a previously undiscovered pocket of primitive stem cells in the spleen that are important for healing several types of damage or injury,” says Denise Faustman, MD, PhD, director of the MGH Immunobiology Laboratory and senior author of the SAGE KE report. “If so, these cells could have much broader therapeutic applications than suggested by our earlier work.”

The successful application and potential uses for adult stem cells continue to grow and expand. Imagine the progress that could be made if the same public support for embryonic stem cell research were directed toward adult stem cells.
Source: bLogicus

Type I diabetes, commonly diagnosed during childhood, is a condition in which the body does not produce insulin. Insulin is a hormone that is used in the body to process glucose by transporting it from blood into cells. Consequently, the disease is marked by chronically high blood glucose levels that over time lead to other health problems such as retinopathy (and blindness), heart disease and neuropathy.
While the cause of Type I diabetes is not completely understood, it is know that the insulin shortage is caused by an autoimmune process in which the body’s immune system destroys the beta cells, the insulin producing cells of the pancreas. The cells are actually spread all over the pancreas in clusters called the “islets of Langerhans” or just Islets.

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