Background

The rise in consumption of refined sugars high in fructose appears to be an important factor contributing to epi-demic of obesity and metabolic syndrome [1]. Fructose is involved in the genesis and progression of the syndrome through deregulation of metabolic pathways in the liver and adipose tissue, as sites of insulin-modulated metabo-lism [2]. Enhanced regeneration of glucocorticoids within the liver and adipose tissue, mediated by the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11bHSD1), may contribute to adiposity and metabolic disease [3]. 11bHSD1 reductase activity is crucially dependent on NADPH, a cofactor generated by the enzyme hexose-6-phosphate dehydrogenase (H6PDH) [4]. We hypothesized that harmful effects of high fructose consumption are mediated by alterations in prereceptor metabolism of glu