The role of dietary fructose in causing diseases such as obesity and fatty liver disease has been controversial. Kylie Kavanagh and her team at Wake Forest School of Medicine (Winston-Salem, NC) studied macaques and vervet monkeys who were allowed to eat as much as they wanted of low-fat food with added fructose for seven years, as compared to a control group fed a low-fructose, low-fat diet for the same time period. The high-fructose group gained 50% more weight and developed diabetes and hepatic steatosis at much higher rates than the control group. Hepatic steatosis is the accumulation of fat in the liver and is an early stage in the development of nonalcoholic fatty liver disease.

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In light of these findings, the researchers decided the next step was to determine whether hepatic steatosis developed because of the animals' weight gain or directly because of the higher fructose consumption. The team carried out another experiment, this time designed to prevent weight gain in the high-fructose diet group. In this study, both groups were fed calorie-controlled diets, one consisting of 24% fructose and the other containing only 0.5% fructose. Though the foods comprising each diet were different, both diets had the same amount of fat, carbohydrates and protein.

After six weeks, the researchers collected blood samples so that they could look for biomarkers of liver damage. Despite maintaining healthy weights, the animals fed the high-fructose diet had more than double the liver damage of the control group (Am. J. Clin. Nutr. published online 19 June 2013; doi:10.3945/acjn.112.057331). The researchers were surprised by how quickly the liver was affected and how extensive the damage was, especially without weight gain being a factor.

Kavanagh and her team also collected fecal samples and performed intestinal biopsies to determine which bacteria were present in the intestine. Live bacteria or bacterial products present in the gastrointestinal tract are passed to the liver in a process called microbial translocation. In the high-fructose group, intestinal bacteria migrated to the liver more rapidly and caused more damage there, suggesting that the fructose somehow caused the intestines to be more permeable.

“Is a calorie a calorie? Are they all created equal? Based on this study, we would say not,” Kavanagh said. The next step will be to test the effects of other sugars, such as dextrose, in addition to fructose to see if they have similar damaging effects on the liver.