Using Sugar to Fight Sugar

A dose of trehalose could halt the effect of fruit sugar, or fructose, Washington University School of Medicine study finds


In the battle against fatty liver disease, could ingesting more sugar be part of the solution?

A new study has found that trehalose, a naturally occurring sugar found in insects and plants, could protect the body against fatty liver disease by blocking the effects of fructose, a sugar found in fruit.

Nonalcoholic fatty liver disease is the accumulation of excess fat in the liver that cannot be broken down, but not as a result of alcohol consumption. According to Harvard Medical School, the liver has shown to convert sugars into fat, and there is evidence that excess sugar consumption is linked to fatty liver disease. Fructose is one of the most common sugars in food and can be found in pastries, cereals and sodas.

Nonalcoholic fatty liver disease affects 30 percent of Americans and about 70 to 90 percent of those who are obese or overweight. While early stages of fatty liver disease can be treated by lowering blood sugar or weight loss, latter stages can result in inflammation in the liver. Inflammation is the body's reaction to foreign threats, and excess inflammation can lead to liver scarring and eventual loss of liver function.

This study consisted of three sets of approximately 10 mice: a control group that was fed a normal diet, a group that was fed a 10-day high fructose diet (60 percent of calories from fructose) and a group that was fed a solution of three percent trehalose with water 48 hours before going on the high fructose diet.

The researchers found that mice who ate the diet with the trehalose treatment did not accumulate fat in their livers, as opposed to those on the high fructose diet alone.

“In general, if you feed a mouse a high-sugar diet, it gets a fatty liver,” first study author Dr. Brian J. DeBosch, an Instructor of Pediatrics at the Diabetes Research Center at Washington University School of Medicine, said in a press release. “We found that if you feed a mouse a diet high in fructose plus provide drinking water that contains three percent trehalose, you completely block the development of a fatty liver."

Not only did the trehalose prevent fructose from entering the liver, but it also broke down fat inside the liver.The trehalose-treated mice also had lower body weight and cholesterol at the end of the study, Dr. DeBosch said.

According to Dr. DeBosch and team, trehalose blocks the transport of energy made from sugar into the liver's cells, thereby starving the cells. That starvation leads the cells to eating their own fat in a process called autophagy. The cells can also eat their own proteins, sugars and other substances. Autophagy could be the mechanism in trehalose that prevented fatty liver disease in this case.

However, the team cannot yet recommend trehalose as a treatment. Trials still have to be conducted on those with actual fatty liver disease, and information needs to be collected on whether the cell starvation is beneficial to those with excess weight or body fat.

"We know the mice that received drinking water with three percent trehalose lost weight, and we suspect that weight loss was due to loss of fat, but we can’t be certain that’s the only effect," Dr. DeBosch said in the release. "We need more studies to make sure they were not losing bone or muscle mass.”

Since more research on the benefits of trehalose are still needed, Dr. DeBosch recommended that those concerned about fatty liver limit sugar consumption, especially from soft drinks.

This study was published February 23 in the journal Science Signaling.

The Washington University Child Health Research Center, Children’s Discovery Institute, Robert Wood Johnson Foundation, AGA-Gilead Sciences Research Scholar Award in Liver Disease, Pediatric Scientist Development Program, Nutrition & Obesity Research Center, Washington University Digestive Disease Research Core Center, Administration and Resource Access Core, Advanced Imaging and Tissue Analysis Core, Murine Models core, American Heart Association, Washington University Spencer T. Olin Fellowship, Washington University NIGMS Institutional Training Grant in Cell and Molecular Biosciences and the Washington University Biomedical Mass Spectrometry Research Facility supported this study.

No conflicts of interest were disclosed.