Dietary fructose is ingested as the simple monosaccharide and also as part of the disaccharide sucrose. Sucrose is hydrolyzed by sucrase at the intestinal brush border to yield one molecule of glucose and one of fructose. Glucose is rapidly absorbed via a sodium-coupled cotransporter and arrives at the liver via the portal circulation. Fructose absorption is accomplished primarily by a fructose-specific hex-ose transporter, GLUT-5. This transporter is found in the jejunum on both the brush border and the baso-lateral membranes. Expression of GLUT-5 increases within hours of exposure to a fructose-enriched diet, indicating that the transporter is regulated by luminal signals. However, consumption of a large amount of pure fructose can exceed the capacity of intestinal fructose absorption, resulting in diarrhea. Several studies have shown that when a single dose of 50 g of fructose is consumed by healthy adults, more than half experience malabsorption, and in some studies malabsorption is also observed with a 25-g dose. Fructose malabsorption results in abdominal bloating, flatulence, and diarrhea. However, the intestinal absorptive capacity for fructose increases when glucose is consumed along with fructose. Thus, coin-gesting glucose to roughly balance fructose, as occurs when most fruits or sucrose is consumed, largely alleviates problems of fructose malabsorption. In addition, fructose absorption increases during sustained fructose consumption, suggesting adaptation to increased fructose intake.
Was this article helpful?