The liver plays an important role in both type 1 and type 2 diabetes. In diabetic patients, the liver makes too much glucose, and muscles and fat are unable to take up or transport glucose so cells can use it.
"We thought if we could find a way to increase the amount of glucose the liver takes out of the blood, and decrease the amount produced by the liver, overall blood sugar levels would decrease," said Alex Lange, associate professor of biochemistry.
This process is dependant on a small regulator molecule, called fructose-2, 6-bisphosphate, that helps control glucose metabolism, or how the body uses and processes sugars.
Using a mouse model, biochemistry research assistant professor Chaodong Wu increased the concentration of the regulator molecule, and found that the mice's blood sugar went down. The mice were using more and producing less glucose.
Wu also noted other changes in the cell that have implications for obesity. When the concentration of the regulator was increased, there were changes in the food intake and overall metabolism. Just like in humans, when food intake is decreased and energy expenditure is increased, weight loss occurs.
Lange said if researchers could find a way to raise the level of this regulator in the liver of humans, for example, by preventing its breakdown, it could lead to a new treatment for diabetes, as well as obesity.
The research was supported by the National Institutes of Health, Minnesota Medical Foundation, and the Minnesota Obesity Center.