"This is a big step forward in dissecting the pathways and mechanisms of diabetes. It is fascinating." Yes the researchers of Yale University have seen a break through in the identification of the missing protein in the adult onset Type II Diabetes mellitus.
They have discovered that mice lacking a gene that produces the enzyme called Akt2 or Protein Kinase B are born without diabetes but develop symptoms of glucose intolerance after two months, roughly the same age that onset begins in humans.
Heading this mission of profound dimension Dr.Kim said that if studies in humans show that the lack of this protein has similar effects, the finding could lead to development of a therapeutic target for preventing Type-2 diabetes.
This study is is supported by Dr. Morris Birnbaum, a Howard Hughes Medical Institute investigator at the University of Pennsylvania Medical school, who devised the "Akt2 knock out mice". In the knockout mice, they discovered a partial defect in insulin-stimulated glucose uptake in the animals' muscle tissue. Further studies showed that the liver of the Akt2 knockout mice did not respond to insulin by lowering glucose production, and their tissues were consuming less glucose in response to insulin.
"This defect in insulin action in the liver and skeletal muscle altered glucose homeostasis throughout the body. Combined with the delayed onset, (it) suggests that Akt2 might have a role in the diabetes. The researchers are correct in stating that the finding presents an opportunity to test potential targets for drug development and hence the gene therapy.
But for the difficulty in using human subjects in such research it is that most adults are unaware they are becoming glucose intolerant until they are diagnosed with Type 2 diabetes at their later age.
Let us hope that future collaborations between the Yale and University of Pennsylvania research teams will result in further understanding the disease.
"This is the future of how we will come to understand the pathology of diabetes."