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Missing Protein Linked to Insulin Resistance in Mice 
WESTPORT, CT (Reuters Health) May 31 - 

In mice lacking Akt2 (also known as protein kinase B), insulin is not able to 
lower blood glucose, which indicates that Akt2 is an essential gene needed to 
maintain normal glucose levels, according to a report in Science for June 1. 
"This is the first time a downstream signaling molecule in the insulin 
pathway has been shown to be needed for normal insulin action," Dr. Morris J. 
Birnbaum, from the University of Pennsylvania, Philadelphia, told Reuters 
Health. In mice engineered to lack Akt2, the researchers found that blood 
glucose was significantly elevated. "Then we measured insulin levels in the 
mice and we found that they were 3- to 5-fold above normal levels. This told 
us that it was likely that the hyperglycemia was due to a defect in insulin 
action," Dr. Birnbaum said. Further experiments revealed that the 
Akt2-deficient mice were significantly defective in their ability to 
stimulate glucose uptake into muscle. "In addition, we found that in the Akt2 
knockout mice, insulin is unable to shut off the pathway of glucose 
production in the liver," Dr. Birnbaum said. "People with type 2 diabetes 
have defects in both glucose uptake into muscle and in regulating insulin 
output in the liver, so simply by eliminating one gene we created a syndrome 
that displays two of the cardinal features of type 2 diabetes," Dr. Birnbaum 
stressed. This does not mean that type 2 diabetes is caused by a defect in 
Akt2; it just means that one can reproduce the phenotype, Dr. Birnbaum 
cautioned. However, "the publication of this paper will allow other 
investigators to take a close look at the role of Akt2 in type 2 diabetes, 
which has not been done before," he told Reuters Health. "In humans," he 
said, "we need to look for mutations linked to Akt genes or to other members 
of the signaling pathway. In the long run, if we are going to design a 
rational drug therapy for individuals with type 2 diabetes we will need to 
map the entire insulin signaling pathway." Science 2001;292:1728-1731. 
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