New Haven, Conn. -- A protein called Akt2 or Protein Kinase B plays an important role in maintaining glucose balance, possibly leading to a drug target for preventing Type-2 diabetes, Yale researchers report in a study published in the June 1 issue of Science.
"When we inactivated the Akt2 protein in study mice, we found that these mice had defects in insulin's action in liver and skeletal muscle, suggesting that Akt2 plays an important role in insulin signaling and action," said Jason Kim, an author on the study and a research scientist in the Department of Internal Medicine at Yale School of Medicine.
"We also found that this defect in liver and skeletal muscle insulin action altered whole body glucose homeostasis, suggesting that Akt2 might have a role in the development of diabetes," Kim added.
Type 2 diabetes is the most common metabolic disease in the world, affecting 120 million people. Insulin resistance plays a primary role in the development of the disease. Kim said diabetes research is now focused on understanding how insulin acts in the body, especially in the area of the insulin signaling pathway. Insulin acts by binding to a receptor that activates a cascade of proteins that are both known and unknown, causing the cells to increase glucose use. The role of the Akt2 protein had been uncertain until co-authors at the University of Pennsylvania provided lab-generated mice with inactivation of the Akt2 protein.
"These mice develop diabetes in a pattern similar to human diabetes and future studies will examine whether a mutation in the Akt2 protein is also seen in people with diabetes," said Kim who is also an associate at the Howard Hughes Medical Institute and a co-director of NIH-Yale Mouse Metabolic Phenotyping Center. "A defect in this protein in humans can explain how diabetes develops."
Other authors on the study included Gerald I. Shulman, M.D. of Yale; Han Cho, Joanne L. Thorvaldsen, Qingwei Chu, E. Bryan Crenshaw III, Klaus H. Kaestner and Morris J. Birnbaum of the University of Pennsylvania; and Marisa S. Bartolomei of the Howard Hughes Medical Institute and the University of Pennsylvania.
Cite This Page: