University of Pennsylvania School of Medicine have discovered a potential new target for a type 2 diabetes drug -- a protein along with its molecular partner that regulates fat metabolism, according to a report in the journal Nature.

“Over the last 10 years, we have begun to understand the importance of fat metabolism in diabetes,” said lead researcher Dr. Morris J. Birnbaum.

When a person eats a meal, the pancreas usually responds by secreting insulin that signals the liver to stop making glucose and burn fat. When a type 2 diabetic eats a meal, insulin cannot stop the manufacture of glucose in the liver, but it can stop the burning of stored fat.

There has been no clear connection until now between insulin and the control of fat metabolism, but Birnbaum's study shows that when insulin is present, the protein Akt2/PKB adds a phosphate group to its molecular partner PGC-1a. When this happens, PGC-1a cannot activate the genes needed for fat metabolism.

The study findings suggest that if a drug could induce Akt2/PKB to add the phosphate group (phosphorylation) to PGC-1a, the liver of a diabetic might be “fooled."

At present, no drugs that target PGC-1a and Akt2/PKB, but Birnbaum said “we hope that drug companies will look for new ways to modify fat metabolism in type 2 diabetics using these possible targets."