Obesity, Insulin Resistance Linked to Body’s Fructose
Over the past few decades, Americans have gotten larger. So large, in fact, that health authorities are now referring to obesity in the U.S. as an epidemic as they battle even childhood obesity numbers. While researchers are searching for a cure, some are also seeking to understand how the U.S. got to this point. A new study published today in the journal Nature Communications could shed some light on how obesity and associated diabetes concerns became so prevalent in the country.
The study shows that both obesity and insulin resistance could be tied to the body’s fructose production, as well as the consumption of fructose. Researchers from the University of Colorado found fructose produced in mice livers from non-fructose carbohydrates (such as glucose) can contribute to the development of obesity and insulin resistance.
“Our studies provide an understanding for why high glycemic foods may increase the risk for obesity and insulin resistance,” said Dr. Richard Johnson, lead author of the study and a professor at the CU School of Medicine. “While some of the weight gain is driven by the caloric content and the effects of stimulating insulin, the ability of high glycemic foods to cause insulin resistance and fatty liver is due in part to the conversion of glucose to fructose inside the body.”
Johnson and his colleagues found that the liver’s process of converting glucose to fructose is at least partially responsible for fatty liver and insulin resistance. The researchers point out that the fructose produced by the body can have an additive effect on sweeteners such as high fructose corn syrup that Americans eat on a regular basis.
“Ironically, our study shows that much of the risk from ingesting high glycemic foods is actually due to the generation of fructose, which is a low glycemic sugar,” said Johnson. “These studies challenge the dogma that fructose is safe and that it is simply the high glycemic carbohydrates that need to be restricted.”