Lanaspa et al. take the matter a step further,
examining the effect of carbohydrate-rich
diets devoid of fructose in KHK-deficient
mice. Intriguingly, these animals were also
protected from the adverse effects of excess
glucose consumption. This makes sense, given
that in the liver the polyol pathway converts
excess glucose into fructose, which is stored
as fat only in the presence of KHK (Fig. 1).
In fact, the authors validate the dependence
of fructose synthesis on this pathway in mice
lacking the polyol-pathway enzyme
aldose reductase; these animals were
also protected from glucose-induced
fatty liver.