Excessive consumption of fructose, a sweetener ubiquitous in the American diet, can result in non-alcoholic fatty liver disease (NAFLD), which is comparably abundant in the United States.
But contrary to previous understanding, researchers at University of California San Diego School of Medicine report that fructose only adversely affects the liver after it reaches the intestines, where the sugar disrupts the epithelial barrier protecting internal organs from bacterial toxins in the gut.
Developing treatments that prevent intestinal barrier disruption, the authors conclude in a study published August 24, 2020 in Nature Metabolism, could protect the liver from NAFLD, a condition that affects one in three Americans.
Fructose is broken down in the human digestive tract by an enzyme called fructokinase, which is produced both by the liver and the gut. Using mouse models, researchers found that excessive fructose metabolism in intestinal cells reduces production of proteins that maintain the gut barrier — a layer of tightly packed epithelial cells covered with mucus that prevent bacteria and microbial products, such as endotoxins, from leaking out of the intestines and into the blood.
Interestingly, the research team found that when fructose intake was reduced below a certain threshold, no adverse effects were observed in mice, suggesting only excessive and long-term fructose consumption represents a health risk. Moderate fructose intake through normal consumption of fruits is well-tolerated.