Since the introduction of high fructose corn syrup in the 1960s, fructose consumption has tripled worldwide. Excess sugar consumption degrades health by contributing to obesity and promoting cancer initiation and progression. Findings of a recent report elucidate the mechanisms by which fructose improves survival of and nutrient absorption by intestinal cells.
Fructose absorption begins in the epithelium (i.e., skin-like cells) of the small intestine, which measures approximately 320 square feet in surface area (about the size of a small studio apartment). This massive surface area is arranged like shag carpet, with structures called “villi” that protrude from the intestine wall. The longer the villi, the greater the surface area and number of intestinal epithelial cells available to absorb nutrients, such as fat or iron. Previous research has shown that fructose can lead to excessive intestinal epithelial growth (called hyperplasia) and cancer; however, the effects of fructose on non-cancerous intestinal epithelial cells is unknown.
The investigators gave mice access to normal drinking water or drinking water with 25 percent high-fructose corn syrup (soda contains about 10 percent) for four weeks. Then they fed mice either a normal diet with no fructose, a high-fat diet with no fructose, or a high-fat diet with sucrose, which contains 50 percent fructose and 50 percent glucose. The researchers measured nutrient composition of the feces and examined the intestinal epithelium for changes.
Mice consuming high-fructose corn syrup in their drinking water showed a 25 to 40 percent increase in intestinal villus length compared to mice consuming normal drinking water. As villus length increased, weight gain and dietary fat absorption also increased. Mice consuming a high-fat diet and fructose gained more weight and had longer intestinal villi than mice consuming a high-fat diet with no fructose, despite consuming and expending the same amount of calories. These mice had less fat in their feces, suggesting an increase in nutrient absorption. The researchers found that intestinal epithelial cells isolated from mice consuming fructose were better able to withstand low-oxygen conditions (called hypoxia), which is a common cause of intestinal cell death.
The authors concluded that high fructose diets increase intestinal villi length and nutrient absorption capacity. These findings provide greater insight into the pathogenesis of intestinal cancer.
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