Honey Component Linked to Obesity

Fructose May Trick You into Thinking You are Hungrier than You Should Be
Biotech Law Weekly, 12/30/05

University of Florida (UF) researchers have identified one possible reason for rising obesity rates, and it all starts with fructose, found in fruit, honey, table sugar and other sweeteners, and in many processed foods.

Fructose may trick you into thinking you are hungrier than you should be, say the scientists, whose studies in animals have revealed its 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, they 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 findings, reported in a recent issue of Nature Clinical Practice Nephrology and in a recent online edition of the American Journal of Physiology-Renal Physiology, add to growing evidence implicating fructose in the obesity epidemic and could influence future dietary guidelines. UF researchers are now studying whether the same mechanism is involved in people. . .

"If you feed fructose to animals they rapidly become obese, with all features of the metabolic syndrome, so there is this strong causal link," Johnson said, "And a high-fructose intake has been shown to induce certain features of the metabolic syndrome pretty rapidly in people."

Now UF research implicates a rise in uric acid in the bloodstream that occurs after fructose is consumed, Johnson said. 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. . .

"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. I think in the next few years we'll have a better feel for whether or not these pathways that can be shown in animals may be relevant to the human condition. . ."