New information on diabetes

Some simple lab mice have been playing a leading role in research that has tried to fit another piece into the puzzle of diabetes treatment.

A team of two Penn and two Yale University researchers have found a link between human type two diabetes and the gene for the protein kinase AKt2 by breeding mice that lacked the gene.

Morris Birnbaum, a professor at Penn's School of Medicine, said scientists have been working for over 20 years to link protein kinases and diabetes.

"It was in the 1970's that people first thought protein kinases would be important to insulin signalling," he said. "But this is the first time a specific protein kinase is actually proven to be required in the insulin process."

The team published their findings in the June 1 issue of the journal Science. Han Cho of Penn's Biology department was the lead writer of the article, while Birnbaum, and Yale graduate students Jason Kim and Gerald Shulman, contributed.

Type two diabetes occurs when sufferers develop a resistance to the insulin produced by their body. The cells in the pancreas that secrete insulin are then unable to compensate by producing more of the substance.

Without insulin, cells are unable to remove sugar -- in the form of glucose -- from the blood stream. The high glucose levels in the blood can lead to cardiovascular diseases, kidney disorders and even blindness.

"The purpose of insulin is to tell the body what to do when there's a lot of food around," Birnbaum said. But in type 2 diabetes, "insulin does not work appropriately," he said.

The research team thought Akt2 was the most promising of three closely related kinase enzymes shared between humans and mice. Birnbaum and his colleagues had also previously noted that Akt2 acted much like insulin when it was overproduced.

To test the theory, the team bred mice that lacked the gene for the protein.

The mice experienced many of the symptoms of diabetes, including elevated blood sugar levels. The mice could not remove sugar from the blood stream, and in fact increased glucose production in their liver cells.

And as the glucose levels rose, the mice produced more and more insulin, but to no avail. The other two kinase enzymes could not compensate completely for the lack of Akt2.

While Birnbaum admits that Akt2 will not solve the problems of all diabetics, it is an important step.

"It's a big, big step closer to being able to identify all the players. It's an incremental process -- if you identify one member it will lead to the next." Birnbaum said.

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