Scientists have discovered a potential new target, Akt2/PKB, a fat metabolism regulatory protein, and its molecular partner, PGC-1a for the treatment of type 2 diabetes.
The study was conducted by a team of researchers led by Morris J. Birnbaum at the University of Pennsylvania School of Medicine.
When a person eats, insulin is secreted by the pancreas to signal the liver to stop forming glucose and burn fat. However in the case of a type 2 diabetic insulin can only do the later job. This gives the diabetic person a 'double whammy' as fatty acids build up from food as well as from liver resulting in more fat deposition in tissues that increase obesity.
As part of the study, researchers conducted experiments on mice to find a direct link between insulin and fat metabolism control.
Researchers found that the protein Akt2/PKB adds a phosphate group to its molecular partner PGC-1a in the presence of insulin after a meal. It results in blocking the activation of the genes by PGC-1a that are required for fat metabolism.
"Muscle and fat tissue also burn fat stores, and we are currently investigating whether PGC-1a and Akt2/PKB have the same role in those tissues," Birnbaum said.
The study also showed that mice that had non-functional Akt2/PKB had low insulin-stimulated phosphorylation of PGC-1a. The researchers showed that excessive PGC-1a or PGC-1a that could not be phosphorylated cause the liver to produce many copies of the fat metabolism genes.
"We hope that drug companies will look for new ways to modify fat metabolism in type 2 diabetics using these possible targets," Birnbaum said.
The findings of the study were published in Nature.