A new animal study may help explain why diets high in the sugar fructose have been linked to insulin resistance, a precursor to type 2 diabetes.

Scientists found that a particular gene, known as PGC-1 beta, appears to play a key role in the development of insulin resistance in response to a high-fructose diet. Rats that had the gene’s activity blocked were protected from insulin resistance despite feasting on a diet loaded with fructose.

A sweetener known as high-fructose corn syrup has been widely used in sodas and processed foods since the 1980s, and some researchers have blamed this trend at least in part for the concurrent rise in obesity and diabetes.

The authors of the current report, in the journal Cell Metabolism, explain that some studies have shown that fructose is metabolized differently than glucose is, being more readily converted into fat.

Other studies have linked diets heavy in high-fructose corn syrup to elevated risks of high triglycerides (a type of blood fat), fat buildup in the liver, and insulin resistance, note Dr. Gerald Shulman and colleagues at Yale University School of Medicine.

For their study on the genetic underpinnings of fructose-induce insulin resistance, they zeroed in on PGC-1 beta because it activates another gene that governs the production of fat by the liver.

When the researchers blocked the gene’s activity in rats fed a high-fructose diet, the animals did not develop insulin resistance and elevated triglycerides.

The implication, according to Shulman’s team, is that inhibiting PGC-1 beta could help treat some cases of high triglycerides, fatty liver disease and insulin resistance. Much more research remains to be done, however.

SOURCE: Cell Metabolism, March 4, 2009.