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Low-cal diet could help diabetes transplants: study
August 30, 2007
www.reutershealth.com
Sticking to a low-calorie, low-sugar diet could help diabetes patients who have been given rare transplants of pancreatic cells, U.S. researchers said on Tuesday.
Tests in rats show that fats literally drown the tender transplanted cells that produce insulin in type-1 diabetes patients who have undergone what is widely known as the Edmonton Protocol. This is the only "cure" for type-1 diabetes.
The study also sheds light on the links between overeating and diabetes, said Dr. Roger Unger of the University of Texas Southwestern Medical Center in Dallas.
If patients avoid processed sugars and overeating in general, they may be able to extend the lives of their transplants and stay off insulin, Unger said.
In type-1 diabetes, the body's immune system mistakenly attacks the insulin-producing islet cells in the pancreas. Patients are unable to produce insulin and must take regular injections for the rest of their lives.
In 2000, a team at the University of Alberta in Edmonton, Canada, reported on a procedure they developed in which patients get transplants of these islet cells into their livers, where they thrive and produce insulin.
The islets are taken from cadavers and it takes several donors to make one transplant. But after a few years, it became clear that the islets were dying off.
About 80 percent of patients needed insulin again after two years.
The assumption was that the body was rejecting the cells, just as an organ is rejected. But Unger did not think so.
"It turned out that if you look at those islets that have been transplanted into the liver, they are surrounded by fat," Unger said in a telephone interview.
RAT TESTS
Writing in the journal Diabetes, Unger and colleagues said they simulated type-1 diabetes in rats by destroying their pancreatic islet cells. They then simulated the Edmonton Protocol with new islet cell transplants.
They found fat built up around the transplanted cells after four weeks. "They were swimming in fat," Unger said. The cells stopped producing insulin and the rats died after 15 weeks.
They repeated the experiment in another group of rats, but put them on a strict diet. And they gave a hormone called leptin to a third group of rats.
These rats fared better.
The problem is likely that the liver's job is to create fatty acids from food, Unger said. "By being too close to the organ that synthesizes the fat, they got a disproportionate hit from the fat," Unger said.
The idea will be easy to test in patients given the cell transplants, he said.
"To test the hypothesis, you wouldn't have to do anything drastic. If you are a kid who has been type-1 diabetic all your life taking insulin and have been on a very strict diet, what is the first thing you are going to do when you get cured? You are going to load up (on treats)," Unger added.
"They want to enjoy it and you can't blame them. I say let them have one good meal and then put them back on the same diet they had when they were on insulin. It won't be popular."
Injections of leptin may also be worth testing in the patients, he said -- as well as the diabetes pill metformin, which helps slow the manufacture of the fatty acids.
Unger said the findings may also help explain why type-2 diabetes develops in adults. It provides a clear biological link to how diabetes could be caused by overeating, he said.
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