Too much sugar can cause liver damage and raise the risk for other medical problems. Now, researchers studying mice have learned that the small intestine protects the liver from exposure to one type of sugar, called fructose. But the small intestine has its limits, the study finds. High doses of fructose overwhelm the intestine’s ability to process the sugar. Researchers reported those results February 6 in Cell Metabolism.
Fructose is a type of simple sugar. It’s found in honey and fruits, as well as in table sugar and in many sweetened foods and drinks. To use fructose for energy, the body needs to convert it into another type of simple sugar, called glucose, or into other smaller molecules. But too much fructose puts a strain on the body. For example, in people it puts the liver at risk for conditions such as fatty liver disease. It also raises the risk of obesity and type 2 diabetes (DIE-uh-BEAT-eez).
Scientists knew fructose could be broken down and absorbed in both the liver and the small intestine. But they believed the liver was mainly responsible for the process. The new study suggests otherwise. It finds that moderate doses of fructose are transformed in the small intestine. The liver steps in only when the dose of fructose is too high for the small intestine to handle.
In that way, the small intestine shields the liver from dangerously high doses of fructose, says Joshua Rabinowitz. One of the study authors, he works at Princeton University in New Jersey. He studies how the body breaks down chemicals.
But how much fructose is too much is still up in the air. Rabinowitz and colleagues fed mice a sugar mix that contained equal parts glucose and fructose. (That’s the ratio in basic table sugar.) Some mice got a lower dose of sugar, and some got a higher dose.
The researchers used a special technique to chemically “label” the sugar molecules they gave to the mice. The method involved swapping certain carbon atoms out for a slightly heavier form of carbon. That allowed the researchers to track which sugars were being transformed and where their by-products were ending up.
Later, the researchers collected samples from different mouse organs. Then they separated out the sugar by-products by weight and identified the molecules with heavier carbon.
At lower sugar doses, researchers found lots of by-products from labeled fructose molecules in the small intestine. But they found only small amounts in the liver. The same was true in the vein that connects the small intestine to the liver. Lots of glucose molecules were found in this vein, though. The chemical labels showed some had been transformed from fructose molecules in the small intestine.
At high sugar doses, the small intestine couldn’t keep up. The vein connecting the intestine and liver had a much higher ratio of fructose to glucose than at lower sugar doses. That suggests the small intestine was passing some fructose along to the liver.
Translating these findings into dietary recommendations for people could be challenging because mice burn more energy relative to their body weight than people do, cautions Luc Tappy. He’s a physiologist at the University of Lausanne in Switzerland. He wasn’t part of the study. He notes that it’s hard to compare sugar doses between humans and mice.
Plus, Rabinowitz adds, scientists don’t know whether the small intestine is a safer place than the liver to process fructose. His lab plans to research that next.