By tricking people into thinking they are hungrier than you should be, scientists at the University of Florida believe that fructose, found in fruit, honey, table sugar and in many processed foods, could play a role in making people fatter.
Studies in animals have revealed that fructose plays a role in a biochemical chain reaction that triggers weight gain and other features of metabolic syndrome - the main precursor to type 2 diabetes.
In related research, the UF scientists also prevented rats from packing on the pounds by interrupting the way their bodies processed this simple sugar, even when the animals continued to consume it.
The researchers are now studying whether the same mechanism is involved in people.
"There may be more than just the common concept that the reason a person gets fat is because they eat too many calories and they don't do enough exercise," said Richard Johnson, professor of nephrology and chief of nephrology, hypertension and transplantation at UF's College of Medicine.
"Our data suggest certain foods and, in particular, fructose, may actually speed the process for a person to become obese."
The findings, reported in the December issue of Nature Clinical Practice Nephrology and in this month's online edition of the American Journal of Physiology-Renal Physiology, add to a growing amount of literature that implicates fructose in the obesity epidemic.
For example, a recent University of Cincinnati study asserted that the body processes high fructose corn syrup (HFCS) differently than other sugars due to the fructose content, leading to greater fat storage.
And last year, researchers at the Harvard School of Public Health claimed in the American Journal of Clinical Nutrition that there was a link between consumption of refined carbohydrates and type 2 diabetes.
However Corn Refiners Association managing director Audrae Erickson told FoodNavigator earlier this year that scientists are wrong to draw a direct comparison between experiments on rats and human consumption of fructose in products such as soft drinks.
And Robert Earl, director of nutrition policy at the US National Food Processors Association, has said in the past that it is incorrect and misleading to suggest the consumption of a specific food or food ingredient was the cause of obesity and the rise of type 2 diabetes. Last year, the US-based Center for Food and Nutrition Policy (CFNP) at Virginia Tech said that there was no reason to believe that humans absorb or metabolise high fructose corn syrup (HFCS), used in beverage applications, any differently than sucrose.
However, the new UF research implicates a rise in uric acid in the bloodstream that occurs after fructose is consumed. That temporary spike blocks the action of insulin, which typically regulates how body cells use and store sugar and other food nutrients for energy.
If uric acid levels are frequently elevated, over time features of metabolic syndrome may develop, including high blood pressure, obesity and elevated blood cholesterol levels.
UF researchers are now studying the uric acid pathway in cell cultures in the laboratory, in animals and in people, and are also eyeing it as a possible factor in the development of cardiovascular and kidney diseases because of its effects on blood vessel responses.
"We cannot definitively state that fructose is driving the obesity epidemic," said Johnson. "But we can say that there is evidence supporting the possibility that it could have a contributory role - if not a major role."