Fructose, the sugar found in fruit, honey and many common sweeteners, may be one cause of the rising obesity rates in the United States.
In animal studies, researchers from the University of Florida have found that fructose tricks your brain into thinking that you are hungrier than you truly are, causing you to eat more to feel satiated. The researchers of the study, published in Nature Clinical Practice: Nephrology, attempt to explain the pathway that fructose takes to make you hungry. In the future, this finding may offer scientists a new way to help people counter weight problems.
“There may be more than just the common concept that the reason a person gets fat is because they eat too many calories.” said Dr. Richard Johnson, the lead author of the study and professor of nephrology at the University of Florida’s College of Medicine.
Following the Fructose Link
While there is no doubt that overeating high-fat, high-calorie foods and forgoing exercise is a major cause of obesity, Johnson’s team tested fructose consumption in animals, hoping to see if this sugar is an underlying cause of metabolic syndrome, a condition that is linked to type 2 diabetes and obesity.
With the introduction of high fructose corn syrup to soft drinks, jellies, ketchup and other commonly used products, fructose consumption has risen more than 30 percent since the 1970s. During this period, the rate of metabolic syndrome and obesity has doubled in the United States, according to Johnson.
To study the link between fructose, metabolic syndrome and obesity, Johnson and his colleagues fed rats a high-fructose diet for 10 weeks. When compared to rats fed a normal diet, the test group had not only gained weight, but there were higher levels of uric acid in their bloodstream, as well as signs of metabolic syndrome.
Johnson said that high levels of uric acid block the action of insulin, a hormone responsible for the proper use and storage of sugar. And without the adequate amount of sugar going to the cells that need it most, the brain thinks that it needs more food to function properly, sending signals to the body to eat more.
“If you feed fructose to animals, they rapidly become obese, with all the features of metabolic syndrome.” said Johnson. “And a high-fructose intake has been shown to induce certain features of the metabolic syndrome pretty rapidly in people.”
But when the researchers blocked or removed the uric acid in the fructose-fed rats, the symptoms of metabolic syndrome were almost completely reversed. “We were able to significantly reduce weight gain.” said Johnson. “The insulin resistance was less, and the blood pressure fell.”
Other studies have provided some evidence that uric acid is a factor in human metabolic syndrome, too, but Johnson cautions that human bodies may not respond to fructose in the same way as rats. He is now beginning a series of studies on humans to determine if fructose plays the same role in weight gain and metabolic syndrome.
“We cannot definitively state that fructose is driving the obesity epidemic.” he said. “But we can say that there is evidence supporting the possibility that it would have a contributory role, if not a major role.”