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Founded in 1957, the HealthPartners ( www.healthpartners.com) family of healthcare companies serve more than one million medical and dental health plan members nationwide. For the third year in a row, HealthPartners is rated one of the best commercial health plans in the nation by U.S. News & World Report/ NCQA’s “America’s Best Health Plans 2007″ andis ranked “Highest in Member Satisfaction among Commercial Health Plans in the Minnesota-Wisconsin Region” by J.D. Power and Associates.

A Dallas-based researcher says he’s pulled off a medical first: successfully treating mice and rats dying of insulin-dependent diabetes without using insulin.

Dr. Roger Unger, chair of diabetes research at UT Southwestern Medical School, is quick to warn that practical applications, if any, are years away. But the research team he headed used high levels of leptin, a substance naturally produced by fat cells, to somehow reverse the otherwise fatal effects of diabetes.

If the experiment is repeated in other labs, and then if leptin can be adapted to treat humans, it might offer the first alternate to the multiple insulin injections used by millions of people who have type 1 diabetes, Dr. Unger said.

How surprising was the result of the experiment?

“It would be like finding aliens landing in your backyard,” Dr. Unger said.

It’s not easy for diabetes to surprise Dr. Unger. He’s been a top researcher for decades with a long list of honors from many major diabetes-related organizations. At 84, he’s still someone that others in the field pay attention to.

His latest findings were published Monday in the Proceedings of the National Academy of Sciences. The paper, titled “Making insulin-deficient type 1 diabetic rodents thrive without insulin,” will get plenty of attention, said Dr. Rohit N. Kulkarni, a researcher at the Joslin Diabetes Center and professor at Harvard Medical School who is also investigating the effects of leptin.

“I think it’s very interesting and intriguing – with an emphasis on the latter,” he said. “It’s quite unexpected.”

Leptin may blunt the short-term impact of Type 1 diabetes – the rapid weight loss and altered blood chemistry that make the untreated disease fatal. It may also help control the longer-term effects of the disease caused by abnormally high levels of sugar in the bloodstream.

But the results reported in this new paper offer almost as many questions as they do answers, Dr. Unger said. And he figures the initial reaction to the results from many other researchers will be negative, “just like mine was,” he said.

Why is it such a surprise? Ever since 1921, when researchers first linked what is now known as type 1 diabetes to a lack of insulin, doctors have assumed that the only successful treatment replaced insulin, usually through multiple daily injections. This new experiment rejuvenated mice and rats without using insulin.

“There’s not a human being who knows anything about diabetes who would have said they would get better without insulin,” Dr. Unger said.

Specialized cells in the pancreas called beta cells respond to the level of sugar in the bloodstream by producing insulin. The hormone has at least two functions:

It acts like a key to a locking gas cap, letting many kinds of cells absorb sugar from the blood to use for fuel.

Insulin also sits on the opposite side of a biochemical teeter-totter from a hormone called glucagon. Glucagon tells liver cells to dump storage supplies of sugar into the bloodstream, providing more fuel as needed. At higher levels, it signals cells to convert amino acids and fats into fuel – basically telling the body to “burn” muscle and fat.

In Type 1 diabetes, which affects about a million people in the United States, the body’s immune system mistakenly kills the beta cells — and the ability of the body to produce insulin.

Without insulin on the other side of the teeter-totter, excess glucagon over-triggers the consumption of muscle and fat, which produces the wasting and rapidly fatal symptoms associated with untreated type 1 diabetes, Dr. Unger said.

In the experiment reported in the new paper, Dr. Unger’s team injected genetically modified viruses that infected the rodents’ liver cells and turned them into leptin-producers.

In a matter of days, the wasting effects of excess glucagon stopped and blood sugar levels dropped near normal. After a few weeks, the leptin levels went down and the blood sugar levels went back up — but not nearly as high as for untreated mice. And the otherwise fatal high-glucagon symptoms never returned, even after almost a year.

A few scientists have thought that leptin was involved with the balance between insulin and glucagon and a few earlier experiments had used leptin along with insulin on rodents, but this is the first to show results without insulin, Dr. Unger said.

“Leptin seems to do everything that insulin does — and with a more prolonged effect,” Dr. Unger said.

Among the many questions left for researchers:

Will the leptin work without the potentially risky modified viruses? The next planned rodent experiment would use simple leptin injections.

Will the effects fade over time? Some of the rodents from the earlier tests are still alive and the researchers are watching.

Does the leptin control blood sugars enough to stave off the long-term effects of diabetes? If not, Dr. Unger says there are other possible adjunct treatments to consider.

But there are no promises that this work will ever produce practical treatments, Dr. Unger said. He’s been disappointed before. In the 1970s, he worked with another protein called somatostatin that seemed to offer a new treatment for diabetes, but the effect was too short-lived.

The bottom line for Dr. Unger is that this research provides new choices for others searching for ways to treat type 1 diabetes.

“Over the years we all began to believe it was insulin or nothing,” he said. “We hope this will open a door that was previously closed and inspire exploration for new and effective alternatives.”

Two experimental treatments suggest new directions for treating diabetes, both using compounds already made by the body, researchers in the United States reported on Monday.

One of the two studies suggests that some current treatments for autoimmune diseases such as the bowel-cramping Crohn’s disease may be taking the wrong approach and doing active harm in some patients.

The two reports, published in the Proceedings of the National Academy of Sciences, each aim to correct some of the things that go wrong to cause type-1 diabetes, which is caused when immune cells mistakenly destroy the cells in the pancreas that make insulin.

The International Diabetes Federation estimates that 230 million people globally have diabetes, and about 10 percent of these have type 1. Patients are usually diagnosed at a young age and must carefully measure blood sugar levels and take insulin for life. There is no cure.

Dr. Denise Faustman and colleagues at Massachusetts General Hospital and Harvard Medical School in Boston tested a cheap generic drug used to prevent tuberculosis, called bacillus Calmette-Guerin or BCG.

Faustman said BCG temporarily elevates levels of an immune system protein called tumor necrosis factor or TNF. Earlier studies had shown that raising TNF in mice can cure them of a condition resembling human diabetes.

“If you are a mouse, we have got you covered. But the ultimate goal is people,” Faustman said.

Her team showed that people with type-1 diabetes have certain numbers of abnormal immune system cells called T-cells. These attack and destroy the pancreatic tissues that normally make insulin.

The tests on blood from 675 people with diabetes and 512 healthy people showed the diabetics had some CD8 “killer” T-cells that could be killed by either TNF or BCG.

“Good” T-cells were not killed by the treatment, they wrote.

The same team is now testing BCG at very low doses in a Phase I clinical safety trial in a few human volunteers.

“Now we have these T-cell markers from blood … so we can know within weeks if we are getting rid of the bad T-cells,” Faustman said.

She said her study suggests that anti-TNF therapies such as etanercept, sold by Wyeth and Amgen under the brand name Enbrel, and Johnson & Johnson’s Remicade may actually cause new autoimmune diseases in some patients with Crohn’s and rheumatoid arthritis.

A second team, at the University of Texas Southwestern Medical Center in Dallas, took a different tack, using a hormone called leptin.

Leptin, only discovered in 1994, is made by fat cells but people with type-1 diabetes often have abnormally low levels of leptin.

Roger Unger of UTSW and colleagues used gene therapy to treat mice with damaged pancreases that made no insulin at all and were dying. They used a virus to carry in genes for leptin, which in turn caused their livers to pump out huge levels of the hormone.

“Within two weeks they were completely normal,” Unger said in a telephone interview. “This was totally unexpected.”

Unger believes the leptin changed the function of another hormone called insulin-like growth factor 1 or IGF1, making it act more like insulin to regulate blood sugar levels.

It may also suppress the unhealthy effects of another compound called glucagon, which is produced excessively in diabetes, he said.

The gene therapy approach would be too risky in people so Unger plans to inject diabetic mice with leptin to see if this works in the same way.