URBANA—A University of Illinois study suggests that dietary fructose affects a wide range of genes in the liver that had not previously been identified.
Most Americans consume quite a bit of fructose—in refined sugars such as sucrose or table sugar (which is half fructose) and in high-fructose corn syrup, used in products as diverse as soft drinks, protein bars and fruit juice. Many scientists believe that high dietary fructose consumption contributes to the development of metabolic syndrome, a group of risk factors that predict heart disease and type 2 diabetes.
“For this reason, it’s important for scientists to understand exactly how consuming high amounts of fructose affects human health,” said the study’s lead author Manabu Nakamura, a UofI associate professor of food science and human nutrition.
Unlike glucose, fructose metabolism occurs mainly in the liver, therefore, Nakamura wanted to gain a complete picture of gene expression in the liver during fructose metabolism.
In Nakamura’s study, 24 rats were fed either a 63-percent glucose or fructose diet four hours a day for two weeks; at the end of this period, half the animals fasted for 24 hours before the scientists performed a gene expression analysis; the other half were examined at the end of a four-hour feeding.
Fructose feeding not only induced a broader range of genes than had previously been identified, there were simultaneous increases in glycogen (stored glucose) and triglycerides in the liver.
“To our surprise, a key regulatory enzyme involved in the breakdown of glucose was about two times higher in the fructose-fed group than in the glucose-fed group,” he said.
The study also suggests that a protein called carbohydrate response element binding protein is responsible for the fructose effect on certain genes that trigger the production of fat, he said.
“We’re continuing to assess the risk of fructose insulin resistance and the consequent risk for development of diabetes,” he said.
