or transplant," said Birnbaum. "We see that Akt1 causes more plentiful, and bigger, β cells they are plump, well fed cells."
The Penn research team, spearheaded by graduate student Robyn Tuttle, began this study to look specifically at the role of Akt1 in living organisms in order to evaluate the proteins possible role in the β cell loss that causes diabetes. Previously, studies of Akt1 in cell cultures determined that the protein had an important role in assisting the function of insulin and helping cells convert glucose into energy. After failing to induce diabetes in their experimental mice by killing β cells, Birnbaum and his colleagues found that there was a significant increase in both β cell size and the total mass of the islets.
According to Birnbaum, Akt1 is a potent factor in deciding the size of cells in mammals. One view is that insulin signaling through Akt1 leads to a coordinated increase in cellular metabolism, which results in bigger cells and an increase in the amount of proteins the cells make. The interplay between insulin and glucose is, in essence, the story of how our bodies derive energy from the food we eat. The Akt1 protein has an important, behind-the-scenes, role in putting that story in motion and coordinating the events.
Perhaps what has surprised the researchers most is how they also see evidence that Akt1 promotes the creation of entirely new β cells.
"The number of β cells that you will have at any given time are determined by three things: how fast they divide, how fast they die, and how fast your body can generate completely new ones," said Birnbaum. "Since the death rate and the division rate did not change in our mice, it is possible that Akt1 also promotes the growth of new β cells."
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Contact: Greg Lester
lesterg@uphs.upenn.edu
215-349-5658
University of Pennsylvania School of Medicine
18-Oct-2001
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