y shows the lack of immune rejection wasn't just an artifact from the strain of rats used for the first experiments.
"In addition, now we also know that this approach works for the much more common type 2 diabetes, something we couldn't predict based on our earlier research," Hammerman says.
One distinction between the two types of diabetes that made such a prediction difficult is the phenomenon known as insulin resistance. Levels of blood sugar are high in type 1 diabetics because insulin-producing pancreas cells have been destroyed. In contrast, blood sugar is high in type 2 diabetics in part because tissues become insensitive or resistant to insulin. The pancreas becomes irreparably damaged in an effort to keep up with the resulting increase in insulin demand.
“The transplanted primordia not only appropriately regulated blood sugar in the type 2 diabetic rats, they also reduced insulin resistance," Hammerman says. "The rats are cured by pig insulin, which comes from the transplants and can be measured in their circulation. The rats’ own insulin-producing cells in the pancreas are atrophied."
As a diabetes treatment for human patients, pig insulin works as well as the human form. However, administering either type of insulin via injection does not control blood sugar well enough to prevent diabetic complications.
In contrast, insulin-producing cells in transplants secrete insulin only in response to elevated blood sugar levels, stopping when glucose levels are normal.
Hammerman and Rogers showed that engrafted embryonic pig pancreatic tissue removed from rats and placed in a test tube releases pig insulin within a minute of being exposed to high glucose levels.
"The link between the glucose-sensing and insulin-releasing machinery of the pig cells is established normally after transplantation of primordia, and they work just like a normal pancreas,” says Rogers.
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