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Penn researchers: Protein may be the essential piece to the pathway by which insulin controls blood sugar

(Philadelphia, PA) Researchers have mimicked the effects of insulin resistance of human type 2 diabetes by creating mice that lack a functional gene for the enzyme Akt2. According to Morris J. Birnbaum, MD, PhD, of the University of Pennsylvania School of Medicine and Howard Hughes Medical Institute, the experiment establishes Akt2, a signaling enzyme also found in humans, as essential for maintaining blood sugar levels. Birnbaum and his colleagues publish their findings in the June 1st issue of the journal Science.

Although most of the biochemical reactions have not yet been defined, researchers believe that insulin causes a series of events initiated by triggering proteins on the surfaces of muscle and liver cells. We have found that Akt2 serves as a crucial gateway for insulin in the pathway to lower blood sugar levels, said Birnbaum, associate director of the Penn Diabetes Center in the Penn Departments of Medicine and Cell and Molecular Biology. When Akt2 does not work, it is like trying to open an office door with a broken lock you wont end up getting much work done.

Type 2 diabetes is a complicated disorder that occurs when sufferers develop a resistance to otherwise perfectly normal insulin. The insulin secreting cells of the pancreas are unable to compensate by making more of the hormone. In healthy individuals, insulin triggers a series of events that allows certain cells to take in sugar, in the form of glucose, from blood. High glucose levels, in turn, can lead to cardiovascular disease, blindness, and kidney disorders.

With a disease such as type 2 diabetes, which affects numerous organs throughout the body, it is difficult to chart out exactly what went wrong a case of too many possible pathways and no clear maps. The difficulty has been compounded by conflicting research on the roles of various proteins within the pathway. Diabetes is a disease that affects multiple organs, so it helps to look at the disease in terms of an entire o
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Contact: Greg Lester
lesterg@uphs.upenn.edu
215 349 5658
University of Pennsylvania School of Medicine
31-May-2001


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