Previous studies have already shown that fructose intake from added sugar is linked with the epidemic rise in obesity, metabolic syndrome, and non-alcoholic fatty liver disease. There is also evidence that fructose intake causes features of metabolic syndrome in animals and humans. This suggests, for instance, if you compared two diets of similar calorie intake, the one with more fructose, as opposed to more starch, will lead to greater accumulation of fat around organs and higher insulin resistance.

By using lab mice, Dr Richard Johnson (senior author and the Chief of the Division of Renal Diseases and Hypertension at the University of Colorado School of Medicine) found that fructose is metabolized by two forms of an enzyme: fructokinase C and fructokinase A.

They discovered that the two forms of fructokinase appear to be responsible for two contrasting effects: one causing fatty liver, obesity, and insulin resistance, and the other protecting against these effects in response to sugar.

"By reducing the amount of fructose for metabolism in the liver, fructokinase A protects against fructokinase C-mediated metabolic syndrome", write the authors, who conclude that "These studies provide insights into the mechanisms by which fructose causes obesity and metabolic syndrome".